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Pathology > Inflammation & wound healing > Flashcards

Inflammation & wound healing Flashcards

1
Q

Describe innate immunity.

A

First line of defence

Non-specific

Rapid onset

No protective immunity

No memory

Phagocyte-mediated

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2
Q

Describe adaptive immunity.

A

Activated

Highly specific

Slower

Protective immunity possible

Memory possible

Lymphocyte-mediated

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3
Q

What mechanical mechanisms feature in the immune system?

A

Body surface: skin, fur Cilia in respiratory tract Air movement in respiratory tract Flushing by liquids: tears, urine, D++ Mucus as barrier

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4
Q

What physiological means aid the immune response?

A

pH changes + extremes Pyrexia kills some infectious agents

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5
Q

What molecular defences contribute to the immune system?

A
  • defensins - lysozyme + sweat gland secretions - myeloperoxidase system - acute phase proteins - complement system - interferons
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6
Q

What cells contain the myeloperoxidase system?

A

Phagocytes

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7
Q

State one role of interferons.

A

Interfere with viral growth

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8
Q

Describe defensins.

A

Small proteins (15-22 AA) Active against bacteria, fungi + viruses Found in many tissues + cells (especially phagocytes + epithelial cells)

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9
Q

Describe lysozymes.

A

Family of enzymes which attack peptidoglycan cell walls of bacteria Secreted in tears, saliva + mucus Sebum from sebaceous glands: waxiness stops bacterial attachment to skin

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10
Q

What are acute phase proteins? What is their biological significance?

A

Proteins whose levels fluctuate in response to tissue injury

May act by binding to organisms + aiding removal by phagocytes = opsonisation

Response is general + non-specific

e.g. C-reactive protein (CRP)

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11
Q

Describe myeloperoxidase and its function within the immune system.

A

Enzyme found mainly in lysosomes in granulocytes + macrophages

Kills bacteria + other pathogens by production of toxic hypochlorite + singlet O2

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12
Q

What is complement? What is the importance of complement?

A

Series of proteins which have multiple protective actions against microorganisms:

  • opsonisation
  • lysis of bacteria
  • recruitment of other cell types to sites of infection
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13
Q

What are interferons? What function do they have within the immune system?

A

Cytokines = intercellular hormones

Significant role in fighting viral infections + tumours

Produced early on in viral infections

IFN-a & IFN-ß produced by virally infected cells

IFN-gamma is produced by activated lymphocytes

Generate antiviral resistance in unifected tissue cells + recruit immune cells

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14
Q

What roles do commensal bacteria offer within the immune system?

A

Inhabit mucosal surface, especially GI + respiratory tract

Also found on skin

Prevent attachment of pathogenic bacteria → blocks their invasion + infection

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15
Q

What type of cells are responsible for ingesting and killing microorganisms?

A

Macrophages

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16
Q

What do mast cells do?

A

Have receptors for IgE ab

Increase vascular permeability

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17
Q

What kind of cell can kill tumour cells, viral infected cells or ab-coated cells?

A

NK (natural killer) cells = form of lymphocyte

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18
Q

Describe the process of phagocytosis.

A
  1. Attachment by non-specific receptors
  2. Pseudopodia forming a phagosome
  3. Lysozyme fusion + killing of microorganism
  4. Release of microbial products
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19
Q

Describe the role of antigens in adaptive immunity.

A

Immune system reacts to presence of ag

Possess epitopes - variable immunogenicity

Antibodies are acquired following prior exposure to ag

Requires lymphocytes

Features: specificity

self/non-self discrimination

memory

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20
Q

Describe the features of adaptive immunity.

A

Memory enables 2º response to same ag

2º response is faster, stronger (better binding + greater response by cells), generates more memory cells

All memory + specificity resides in lymphocytes populations

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21
Q

What role do eosinophils play within the immune system?

A

Anti-parasite immunity

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22
Q

What function do polymorphonuclears + monocytes have in the immune response?

A

Phagocytosis

Ag presentation

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23
Q

What 2 kinds of adaptive immunity are there? What agents mediate these kinds?

A

Humoral immunity - mediated by B-lymphocytes

Cellular immunity - mediated by T-lymphocytes

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24
Q

What are the major internal lymphoid organs?

A

Thymus

Bone marrow

Spleen

Lymph nodes

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25
Q

State the major surface lymphoid organs.

A

Salivary glands

Respiratory tract

Mammary glands

Intestines

Urogenital system

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26
Q

What 4 sites of lymphocyte development are there?

A

Thymus

Bone marrow

Peyer’s patches

Bursa of Fabricius (only found in chickens)

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27
Q

Give 5 examples of sites in the body where lymphocytes respond to ag.

A

Tonsils

Spleen

Lymph nodes

Peyer’s patches

Bone marrow

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28
Q

Where in the body do T-lymphocytes mature? And B-lymphocytes?

A

T-lymphocytes mature in thymus

B-lymphocytes mature in bone marrow

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29
Q

What does humoral immunity entail? What kind of lymphocytes are involved?

A

Production of ab

Involves B-lymphocytes

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30
Q

What happens with cell-mediated immunity? What type of lymphocytes are involved?

A

Produces cytotoxic effects

Requires T-lymphocytes

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31
Q

What two different categories of lymphoid organs are there? Describe them.

A

1º (central) lymphoid organs

  • where B- + T-lymphocytes mature into ag-recognising cells
  • lymphocytes acquire ag-specific receptors

2º (peripheral) lymphoid organs

  • ag-driven lymphocyte proliferation + differentiation
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32
Q

Describe the thymus. How does the adult organ differ from the developing thymus?

A

Small thoracic organ near to heart

Site of T-lymphocyte maturation + selection

Lymphocytes are transported to thymus via blood

Active in young animals, then shrinks + atrophiesm producing fewer T-cells

Contains Hassal’s corpuscles

Adult: contains many fatty + atrophied areas

still functional; greatly reduced in size

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33
Q

Describe the thymic structure.

A

T-lymphocytes are in intimate contact with epithelial cells - useful for selection

Immature T-lymphocytes mature within thymus cortex

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34
Q

What percentage of T-lymphocytes survive the ‘thymic journey’?

A

Only 5%

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35
Q

What are Hassal’s corpuscles?

A

Composed of flat non-secreting epithelial cells arranged in concentric keratinised layers

Seen in medulla of thymus

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36
Q

What does the cortex of the thymus contain?

A

Densely populated with immature T-lymphocytes of various sizes

Scattered macrophages - removing apoptotic lymphocytes

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37
Q

Where does thymic selection of T-lymphocytes occur? Describe the process.

A

Having migrated from the cortex to the medulla, T-lymphocytes encounter macrophages and dendritic cells

These cells perform thymic selection ⇒ mature functional T-lymphocytes

These then enter the circulation + migrate to 2º lymhoid organs where they encounter + respond to ag

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38
Q

What types of cells do immature T-lymphocytes have to navigate past in order to survive thymic selection to reach maturity?

A

Enter thymic cortex: encountering thymocytes + cortical epithelial cells

Within medulla: they encounter medullay epithelial cellsm dendritic cells + macrophages

This selection process removes most of self-reactive T-lymphocytes

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39
Q

Where do dendritic cells originate from?

A

Bone marrow

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40
Q

Describe the Bursa of Fabricius.

A

Only found in birds

Is an organ located near the cloaca

Site where B-lymphocytes undergo maturation → ab-producing B-lymphocytes

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41
Q

What route does lymph take within the body?

A

Fluid filters from capillaries and drains into lymphatic vessels to become lymph

Lymph eventually drains into venous blood after passing through 2º lymphoid organs

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42
Q

What functions does lymph have?

A

Drains interstitial fluid

Transports dietary lipids

Facilitates immune responses by draining ag from tissues to lymph nodes, and eventually blood

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43
Q

Where do the lymph nodes receive lymphocytes from?

A

10% from lymph

90% from circulation, entering via high endothelial venules

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44
Q

Describe the features of lymph nodes.

A

Highly efficient at trapping ag entering via afferent vessels

Lymphocytes are retained for up to 24hrs

ag react with macrophages, T- & B-lymphocytes → immune response

Composed of cortex → paracortex → medulla

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45
Q

What constituents form a lymph node?

A

Germinal centres

Subcapsular sinuses

1º & 2º follicles

Associated artery + vein

Dividing trabeculae + medullary cords

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46
Q

Describe the structure of the spleen.

A

Red pulp = open sinusoids containing RBCs

White pulp = mainly composed of lymphocytes

Red pulp surrounds white pulp

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47
Q

What does MALT (mucosa-associated lymphatic system) comprise?

A

Tonsils

Peyer’s patches

Appendix

  • very dense areas of lymphocytes
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48
Q

Where are MALT areas found?

A

Found in many areas of GIT, respiratory tract and genito-urinary tract

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49
Q

Describe the tonsils.

A

Lacks a capsule or afferent lymphatics

Have lymphoid follices + germinal centres

Found in vatious forms around upper respiratory tract

Contain lymphocytes and macrophages

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50
Q

Describe the features of Peyer’s patches.

A

Found in ileal submucosa of SI

Visible to naked eye

Germinal centres prominent as sites of ab-production

Detect ag that diffuse across intestinal epithelia via M-cells

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51
Q

What hormones are produced by the thymus to support T-lymphocytes growth and differentiation?

A

Thymosin

Thymulin

Thymopoeitin

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52
Q

What is an epitope?

A

The immune reactive part of an antigen

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53
Q

Define an antigen.

A

Any agent that is capable of binding specifically to components of the immune system.

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54
Q

What is an immunogen?

A

Any agent capable of inducing an immune response.

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55
Q

What are the key interactions needed for ab-production?

A

Ag + specific lymphocyte

Lymphocytes with each other + accessory cells

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56
Q

What is the humoral defence composed of?

A

B-lymphocyte + ag → ab-production (plasma cell)

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57
Q

What is a plasma cell?

A

A fully differentiated B-lymphocyte which produces a single type of ab

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58
Q

Describe the process of achieving humoral immunity.

A

Clonal expansion occurs when ag meets small resting lymphocyte

Lymphocyte multiplies + matures

Activated, expanded B-lymphocytes become plasma cells - exit lymphoid tissues and migrate to areas of infection to secrete ab

Some lymphocytes become memory cells instead to enable a strong 2º immune response on re-challenge

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59
Q

Describe the structure of a basic immunoglobulin.

A

Symmetrical unit comprised of 2 heavy chains + 2 light chains

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60
Q

How many different classes of heavy immunoglobulin chain are there? Name them.

A

5 different classes:

IgM = micro

IgD = delta

IgG = gamma

IgA = alpha

IgE = epsilon

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61
Q

What fragments constitue an Ig molecule?

A

Fab = fragment ag binding

Fc = fragment crystallisable

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62
Q

What kind of bond is present between heavy-heavy and heavy-light chains of Ig molecules?

A

Disulphide bridges

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63
Q

What can both heavy and light chains be further sub-divided into?

A

Constant and variable regions of heavy chain

Constant and variable regions of light chain

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64
Q

At what region do ab bind to ag?

A

Variable regions of light and heavy chains

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65
Q

What is the name of the section of the Ig molecule between the Fac and Fc regions?

A

Hinge region

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66
Q

What is another name for the antigen binding site on an Ig molecule?

A

Hypervariable region = actual ag bindingsite on Ig, found in variable region

* this will bind epitope of ag

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67
Q

What part of an Ig molecule dicatates its biological function?

A

Heavy chain end of Ig molecule

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68
Q

How is IgA transported across mucosal epithelium?

A

Via a transport vesicle that utilise secretory component

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69
Q

What does the valency of interaction between ag + ab depend on?

A

Number of ag being bound by ab

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70
Q

What is another term used for the valency of interaction between ag + ab?

A

Avidity = overall binding strength between an ab + ag

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71
Q

What are antisera?

A

A blood serum containing ab against specific ag

Injected to treat or protect against specific diseases

Polyclona as many epitopes stimulate many B-lymphocytes

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72
Q

What type of cells produce ab? Where do ab generally terminate?

A

B-lymphocytes produce majority of ab

Ab tend to end up in fluids

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73
Q

What different forms of ab are there?

A

Soluble and membrane-bound forms

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74
Q

What are Ig produced by and in what situation?

A

Produced by B-lymphocytes that have been expose to ag

Ig are specific to ag

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75
Q

What are the 4 phases of a 1º antibody response?

A
  1. Lag phase
  2. Log phase
  3. Plateau
  4. Decline
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76
Q

What is antibody switching? Describe the process.

A

Following first encounter with ag, B-lymphocyte secretes IgM

Lots of memory cells are also generated - many of these have switched from IgM ⇒ IgG (or IgA) expression

Upon 2º response, secretion of high affinity ab which is mainly IgG in most tissues

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77
Q

What is the theory behind vaccination?

A

That 1º immune responses will generate memory cells + protection through 2º ab response

= acquired immunity

* mimics 1º infection

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78
Q

State the different funtions of antibodies.

A
  • Prevent pathogen attachment

invasion of host cells

replication

toxin production

  • Activate complement system
  • Opsonisation by Fc + complement receptors
  • Cytotoxic for pathogen + infected cells (NK)
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79
Q

What happens in the body between 1º and 2º immune responses?

A

Animal learns which ab is most effective - regulated by specficity of lymphocytes

* antibody switching

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80
Q

What is complement comprised of?

A

System of proteins - normally inactive molecules that are activated in series (through a cascade)

Mainly produced by liver

Mainly found in body fluids including circulation

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81
Q

What are the problems associated with complement?

A

Its capacity to harm the host:

e.g. swelling of joints

canine rheumatoid arthritis- disruption of hyaline cartilage

  • cell lysis
  • attraction of phagocytes to site of ab production/localisation
  • induction of anaphyltoxins in tissues
  • activation of phagocytes + mast cells
  • smooth muscle contraction
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82
Q

What mechanisms of protection does complement have?

A
  1. Opsonisation
    - bind to pathogen to promoto phagocytosis by phagocytes bearing complement receptors
  2. Chemoattractant
    - recruits phagocytes in situ
  3. Lysis
    - damages certain bacteria by perforating membrane
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83
Q

How does amplification work within complement activation cascades?

A

Each stage of complement is a substrate which becomes an enzyme on activation, whose substrate is the next complement stage

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84
Q

Name the 3 pathways that result in complement activation.

A

Classical pathway

Lectin pathway

Alternative pathway

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85
Q

Describe the classical pathway.

A
  1. IgG or IgM antibody binds to an antigen
  2. Complement component C1q binds to ag-bound ab
  3. C1q activates C1r → activates C1s → C1s binds + cleaves C2 + c4
  4. C2a + C4a split off
  5. C2b + C4b attach to protein close to ab - repeated many times, freeing complexd to actiave further molecules
  6. C3 binds to C2b → C3a splits off
  7. C3b splits many copies of C5 → each C5 binds to nearby C2b + C4b
  8. C5b is target for binding of C6, C7, C8+ C9
  9. C5b-C9 forms membrane attack complex → penetrates cell membrane, allowing ionic leakage
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86
Q

What are the components of a membrane attack complex?

A

C5b

C6

C7

C8

C9

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87
Q

What is result of the classical complement pathway?

A

Complement-mediated lysis

H2O + ions enter cell → cell to swell + lysis

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88
Q

Which component of the classical pathway is also crucial to the other pathways?

A

C3

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89
Q

What is C1 molecule comprised of?

A

C1q

C1r

C1s

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90
Q

What is another name for the lectin pathway?

A

MBL pathway = mannan-binding lectin

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91
Q

What is needed for the MBL pathway?

A

A pattern recognition receptor

= protein produced by liver

  • recognises patterns on infective processes
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92
Q

Describe the lectin pathway.

A
  1. Initiates complement cascade by bindign to pathogen surfaces
  2. Cleaves C2 + C4 to activate C3
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93
Q

What potential factors can initiate the alternative pathway of complement activation?

A

Pathogen components

  • many gram- bacteria
  • lipopolysaccharides from gram- bacteria
  • many gram+ bacteria
  • fungal cell walls
  • some viruses + parasites

Non-pathogens

  • complexed IgG + IgA
  • anionic polymers
  • pure carbohydrates
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94
Q

What are the various outcomes for activation of C3?

A

C3a is produced:

  • when combined with C5 ⇒ inflammatory response
  • mast cells are degranulated → increases vascular permeabilty

C3b is also produced:

  • opsonisation - C3b remains on microbial cell wall + is recognised by phagocytes → phagocytosis
  • lysis - C3b activates C5 → formation of membrane attack complex → cell lysis
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95
Q

What does degranulation of mast cells result in the release of?

A

Histamines

Heparins

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96
Q

How can the process of opsonisation be improved in its efficiency?

A

Binding of activated complement via C3

Binding of ab (Fc)

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97
Q

What causes mast cells to degranulate?

A

Binding of C3a + C5a

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98
Q

What are C3s + C5a known as?

A

Anaphylatoxins

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99
Q

What local events are associated with anaphylatoxins (C3a + C5a)?

A
  • increased vascular permeability
  • adhesion + chemotaxis of neutrophils + monocytes
  • smooth muscle contraction
  • degranulation of mast cells
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100
Q

What is chemotaxis?

A

The process by which phagocytes are attracted to the site of inflammation.

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101
Q

Which of the complement components has the greatest potency?

A

C5a > C3s > C4a

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102
Q

What are the biological functions of the complement components C3a, C4a & C5a?

A

Increased vascular permeability → increased fluid leakage from BV, extravasation of Ig + complement molecules

Increased cell adhesion molecules

Increased migration of macrophages, PMN leucocytes + lymphocytes

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103
Q

What does extravasation refer to?

A

The leakage of fluid from within a contained area

e.g. blood vessel

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104
Q

Which complement functions are dependent on the activation of C3?

A
  1. Lysis
  2. Opsonisation
  3. Activation of inflammatory response
  4. Clearance of immune complexes
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105
Q

What happens to macrophages and neutrophils following the process of phagocytosis?

A

Macrophages persist

Neutrophils are end-stage cells that die having consumed the foreign body or microbe

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106
Q

Name the different complement control mechanisms.

A

Lability - self-destruct ifthey do not achieve activation over a certain distance

All cells have surface protection provided by specific complement receptor proteins

Factor I: cleaves C3

Factor H: cleaves C3

C1 inhibitor: binds C1r + stops C2 & C4 from binding

C3b receptor on RBCs

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107
Q

What are PAMPs?

A

Pathogen-associateed molecular patterns

= molecules on pathogens recognised by receptors on cells of innate immue response.

e.g. bacterial lipopolysaccharide

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108
Q

What are PRRs?

A

Pattern recognition receptors

= primitive part of immune system, found on phagocytes + mast cells, these identify + bind PAMP

* no memory

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109
Q

What are monocytes?

A

Large phagocytic WBC with a simple oval nucleus + clear, greyish cytoplasm

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110
Q

Define a macrophage.

A

A large phagocytic cell found in stationary form in the tissues, or as a mobile WBC especially at sites of infection

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111
Q

What is a mast cell?

A

A cell filled with basophilic granules, found in numbers in connective tissue and other substances during inflammatory + allergic reactions

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112
Q

What proportion of B- and T-lymphocytes are seen in the circulation?

A

B-lymphocytes at 20%

T-lymphocytes at 80%

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113
Q

How many different kinds of T-lymphocyte are there? What are their functions?

A

Helper T-lymphocytes - assist both ab-production + cytotoxic T-lymphocyte effects; associated with CD4

Cytotoxic T-lymphocytes - kill infected host cells + tumours; associated with CD8

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114
Q

What kind of lymphocytes are associated with CD4?

A

Helper T-lymphocytes

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115
Q

What kind of lymphoctes are associated with CD8?

A

Cytotoxic T-lymphocytes

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116
Q

How do T-lymphocytes recognise ag?

A

Through specific receptors = TCR (T-cell receptors)

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117
Q

What are TCR composed of?

A

Variable + constant domains

Single ag-binding site

a- + ß-chains

CD3 complex

Accessory molecule of CD4 or CD8

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118
Q

How does a B-lymphocyte ag-receptor compare to a T-lymphocyte ag receptor?

A

B-lymphocyte receptor - binds surface Ig

2 identical ag recognition sites

T-lymphocyte receptior - 1 ag recognition site

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119
Q

What is the importance of B-lymphocyte development in the bone marrow?

A
  • regulate construction of an ag-receptor
  • ensures each cell has only 1 specificity
  • checks + disposes of self-reactive B-lymphocytes
  • exports useful cells to periphery
  • provides a site for ab-production
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120
Q

Describe the process of removing self-tolerant B-lymphocytes.

A

Clonal deletion

  • small pre-B cell assembles Ig
  • immature B-cell recognises multivalent self-ag
  • clonal deletion occurs by apoptosis
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121
Q

What is an MHC (major histocompatibility complex)?

A

Cell surface molecules used for tissue typing in transplantation

Defines an individual molecularly

MHC genes code for expresses membrane proteins

Highly polymorphic

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122
Q

What are the functions of MHC?

A

Cell communication within immune cell populations

Control type + degree of immune response

MHC proteins present ag to T-lymphocytes

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123
Q

What are the distinguishing features between the different classes of MHC?

A

Class 1: expressed on most nucleated cells

presents proteins to CD8+ cytotoxic T-cells

Class 2: expressed on APCs, macrophages, B-cells + activated T-cells

presents proteins to CD4+ helper T-cells

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124
Q

Describe the different selection processes that occur in the thymus affecting T-lymphocyte maturation.

A

Positive selection:

T-cells that can react to self MHC carrying peptides are allowed to live.

Those that cannot undergo apoptosis

Negative selection:

T-cells that react strongly to self-ag are eliminated.

* only T-cells that can react to MHC but do not bind strongly to self-ag emerge as mature T-cells

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125
Q

What are the functions of mature T-lymphocytes?

A

Cytotoxic to infected cells = CD8

Activate macrophages = CD8

Help ab-production by B-cells = CD4

cytotoxicity by other T-cells = CD4

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126
Q

What is the significance of APCs (antigen-presenting cells)?

A

Expresses ag to helper T-cells → proliferate

Cytotoxic T-cells will kill these cells

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127
Q

What are the 3 main types of APC?

A

Dendritic cells

B-lymphocytes

Macrophages

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128
Q

Describe the main features of APCs.

A

They lack ag-specific receptors

Process + present ag to T-lymphocytes so that they can react

Present ag via MHC on their surface

Capable of killing own cells if infected

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129
Q

Describe the components needed for T-cell recognition of ag.

A

MHC molecule present peptide

Ag is peptide-bound to molecule

TCR recognises MHC + peptide

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130
Q

What is the role of cytokines?

A

Control of immune responses

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131
Q

What are cytokines? What is the name given to those are produced by leucocytes?

A

Intercellular hormones

Interleukins - produced by one leucocyte to affect another

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132
Q

Which of the APC is the most effective + most potent?

A

Dendritic cells

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133
Q

How do the TH1 and TH2 reaction pathways affect one another?

A

They are antagonistic

Inhibitory effect determined by cytokine production

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134
Q

What is the role of NK cells?

A

To recognise cells lacking in MHC class 1

Effective vs. tumours, some viruses

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135
Q

Which MHC class presents ag to helper T-cells?

A

Class 2 - assists ab-production + cytotoxic T-cell activity

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136
Q

Which of the classes of MHC presents ag to cytotoxic T-lymphocytes?

A

Class 1 - enables killing of infected host cells

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137
Q

What different pathways are there for processing ag?

A

Endogenous pathway

  • host cells process infective agents + express on cell surface with MHC class I
  • targeted by Tc - host cell is killed

Exogenous pathway

  • macrophages digest infective agent + produce peptides to present on surface MHC II
  • or to be picked up by other cells (e.g. dendritic cells) to be presented to Th cells to activate them
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138
Q

By which pathway can all APICs present ag to Th cells?

A

Exogenous ag can be presented

Using MHC II

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139
Q

Which of the APCs tend to process ag (via endogenous pathway)?

A

Macrophages

Dendritic cells

140
Q

What type of APCs tends to present ag?

A

Dendritic cells - circulate around body + localise in lymph nodes

141
Q

Describe the process of ag-processing.

A

Usually needed to degrade large proteins or organism prior to presentation by APC

Not all degradation is performed by APC

All APC can present ag in association with MHC I

142
Q

State an advantage + a disadvantage of dendritic cells as APCs.

A

Advantage: excellent + highly potent APC

Disadvantage: poor at processing large ag

143
Q

What happens when T-lymphocytes are activated?

A

Blast cells are generated

IL-2 receptor expression is increased

IL-2/4 synthesis is increased

  • drives clonal proliferation ⇒ many effector +/- memory cells
144
Q

What different kinds of helper T-lymphocyte are there?

A

TH1 - assist T-lymphocyte functions (Tc + macrophage activation) for intracellular infections

TH2 - assist B-lymphocytes to make ab for extracellular infections

145
Q

How do cytotoxic T-cells respond to ag?

A

Identify ag-presentation by MHC I on infected cells ⇒ induces apoptosis within target cells

146
Q

How do NK cells respond?

A

Are cytotoxic lymphocytes that recognise cells without MHC I - commonly seen with tumours + some virally infected cells

Induces apoptosis within target cells

147
Q

How do immune cells communicate?

A

Through direct cell-cell contact induced by peripheral lymphoid tissues trapping and concentrating ag-containing phagocytic cells

148
Q

What are the 4 phases of immune responses?

A
  1. Recognition phase
  2. Activation phase
  3. Effector phase
  4. Memory phase
149
Q

Describe the effector phase of an immune response.

A
  • lymphocytes are specifically activated to perform functions for eliminating ag
  • work with other non-lymphoid effector cells (neutrophils, phagocytes)
  • complement - lysis + phagocytosis of microbes
  • cytokines - enhance function of phagocytes + other lymphocytes; stimulate inflammation
150
Q

Describe the recognition phase of the immune response.

A

Binding of foreign ag to specific receptors on mature lymphocytes

151
Q

Describe the memory phase of an immune response.

A

Lymphocytes with a high affinity for ag are in the correct site if a repeat infection should occur with the same ag

152
Q

Describe the activation stage of an immune response.

A

All lymphocytes undergo proliferation + differentiation

Lymphocytes migration to sites of ag entry and persistence

153
Q

What factors regulate an immune response?

A

Ag

Ab

MHC genes

Lymphoyctes e.g. Treg

154
Q

What is Treg?

A

A CD4 (helper) lymphocyte

155
Q

Describe Treg and its role within an immune response.

A

Has surface CD4 + CD25

Switches off immune response - regulatory role

Prevents state of autoimmunity

Selected in thymus

156
Q

Describe passive immunity.

A

Offers short-term protection as ab wane wiithin recipient

No cell-mediated immunity; ab only

Risk of hypersensitivity with foreign serum

Blocks inducation of active acquired immunity

157
Q

Where is passive immunity acquired from?

A

Natural: MDA in colostrum or via placenta

Artificial: injection of ab (sera) from resistant ⇒ suscpetible animal

158
Q

By what means is active acquired immunity achieved?

A

Natural infection

Artificial immunisation: living organisms vs dead vaccines

159
Q

What is the main concern with vaccinating animals?

A

That they may not be able to withstand 1º infection

160
Q

What does an anamnestic response refer to with regards to passive immunity?

A

Refers to the enhanced reaction of the body’s immune system to an ag which is related to one previously encountered

161
Q

Which of the Ig molecules provide the main protective ab?

A

IgG or IgA

162
Q

What should an ideal vaccine do?

A

Provide prolonged strong immunity

Immunity sholud be conferred to any foetus carried

Free of side effects

Cheap, stable + easy to apply

Produces immunity distinguishable from natural infection (DIVA)

163
Q

What are the essential components to a vaccine?

A
  • stimulation of APCs
  • both B + T cells stimulated
  • helper + effector responses to several epitopes
  • vaccine ag should persist in appropriate sites in lymphoid tissues
164
Q

State the reasons for avoiding vaccination.

A
  • poor natural/artificial immunity offered
  • immunity doesn’t prevent infection → carrier state
  • ab contribute to disease
  • vaccine causes disease by infection
  • vaccine ag interferes with serodiagnosis
165
Q

What are the disadvantages of killed vaccines?

A
  • less immunogenic than live vaccines
  • have to be administered more often
  • not effective by natural infection route
  • require adjuvant for effective immunity
166
Q

By what methods can pathogens be modified to attentuate them for use in vaccines?

A

Heat

Culture

Chemical

167
Q

What are the advantages to using killed vaccines?

A

Safer than attenuated vaccines

Give better ab responses compared to cell-mediated immunity

168
Q

How can a virus be attentuated for vaccine usage?

A

Pathogenic organism with gene for virulence factor

  • virulence gene removed - deletions, knock-outs
  • avirulent organism lacking gene for virulence factor is placed into vaccine
169
Q

What are the different routes for administering vaccines?

A

SC

IM

IN

Aerolisation

Water

Feed

170
Q

What are the benefits of subcutaneous vaccines?

A

Skin contains specialised, monocyte-derived epidermal cells

= Langerhans cells - precursors of dendritic cells

  • capture + process ag in skin
  • travel in lymph to lymph node → follicular dendritic cells
  • stimulate T-cells very effectively
171
Q

What is the significance of adjuvants within vaccines?

A

Added to increase effectiveness of killed vaccines

  • promote APCs
172
Q

State 4 reasons why vaccinations might fail.

A

Incorrect administration

Wrong time period

Wrong vaccine used

Insufficient quantity of vaccine used

Passive immunity still efficacious

173
Q

What is one of the problems, seen in particular with cats + FeLV vaccination? How is this dealt with?

A

Post-vaccinal sarcoma - relatively rare

With FeLV vaccine, this is injected into muscle of HL as this is easier to amputate should a sarcoma result than one localised to the scruff of the neck

174
Q

What is the basic outline for foetal immunology?

A

Thymus appears first

2º lymphoid organs develop

Cell-mediated immunity develops at same time as ab production

175
Q

How do the levels of macrophages + PMNs in neonates compare to levels in the adult?

A

PMN - similar level + function in neonate to adult levels

Macrophages - phagocytic ability impaired

* thought to be due to increase in glucocorticoids - may also impair abilities of APC

176
Q

What does tolerance refer to?

A

A lack of immune response to specific ag

177
Q

By what means does transfer of immunity to offspring occur?

A
  • Placental transfer - primates receive IgG only
  • 5% placental: 95% colostral - dogs, cats
  • 100% colostral - ruminants, pigs, horses
178
Q

What is the organ responsible for supplying mammary glands with Ig?

A

Supramammary lymph nodes ⇒ mammary ducts

179
Q

How does Ig reach colostrum from the circulation?

A

Specialised FcR in mammary gland draws ig from serum to add to colostrum

180
Q

What is the minimum amount of colostrum needed by calves + foals within 6hrs of birth?

A

1L colostrum minimum

181
Q

How does absorption of colostrum occur?

A
  • ingested and passes into GIT where enzyme levels are low/blocked so that proteins can reach SI
  • neonates have specialised Fc receptor on intestinal epithelia for brief period following parturition
  • Igs are bound, actively pinocytosed → reaches circulation + lymphatics
182
Q

At what point following parturtition do circulating Igs reach their peak?

A

12-24hrs post-partum

183
Q

When is the greatest risk of infection posed to newborn animals?

A

In between decline of passive immunity + stimulation of active immunity of immue system

184
Q

By what means can colostrum be assessed?

A

Hydrometer/colostreter - measures specific gravity to correlate with TP or Ig content

Refractometers - measures protein content through degree of light refraction

185
Q

Describe the test used to making a rapid assessment of Ig levels in foals.

A

Zinc sulphate turbidity test

  • the cloudier the solution, the greater the concentration of Ig

Radial immunodiffusion (RID)

  • measures foal serum Igs
  • failure of passive transfer = when IgG < 2mg/mL
  • partial transfer = when IgG 2-4 mg/mL
  • adequate transfer = when IgG > 4 mg/mL
186
Q

At what serum concentration is failure of passive transfer deemed to have occurred? What concentration is considered adequate? And partial transfer?

A

< 2 mg/mL for failure of passive transfer

2-4 mg/mL is partial passive transfer

> 4 mg/mL is adequate transfer

187
Q

What means of Tx are there for FPT?

A

Provide additional colostrum:

  • bottle or nasogastric tube
  • only suitable for neonates up to 15hrs old

Over 15hrs old:

  • * no oral absorption is occurring*
  • use IV plasma - commercially available with high specific ab titres
  • both IV plasma + commercial plasma must be free of anti-erythrocyte ab
188
Q

What are the different considerations for treating FPT?

A

Age of foal - affects course of Tx

If younger than 15hrs, give additional colostrum via nasogastric tube or bottle

If older than 15hrs, requires IV plasma - from healthy animal to provide sera Igs

189
Q

Describe CMI in colostrum.

A

Many lymphocytes present - mostly T

May survive up to 36hrs in intestine of neonate calf

Some penetrate to local lymph nodes → circulation

Enables some CMI + humoral immunity

190
Q

Why would non-suckled calves produce ab sooner than suckled calves?

A

MDA inhibit ab production

191
Q

Describe the normal neonatal immune response.

A

GI lymphoid tissue responds well to ingested ag

Passive immunisation inhibits development of immune response

192
Q

What is the 1/2 life of cat + dog ab in their neonate offspring?

A

8-10d

193
Q

How is passive immunity achieved in the chick?

A

Serum IgG is transferred from serum to yolk within ovary

IgM + IgA are picked up in oviduct - remain within albumin to be ingested by neonate chick

194
Q

What kind of relationship does commensalism describe?

A

A neutral relationship

195
Q

What term is used to describe the occurrence of symbiotic pathogens becoming pathogenic if weakness occurs in host animal?

A

Opportunistic pathogens

196
Q

What are the distinguishing features of prokaryotes?

A

No defined nucleus

Cell lacks compartmentalisation

Only have one circular chromosome

197
Q

Describe the difference between gram+ and gram- bacteria.

A

Gram+

Appears purple when stained with crystal violet

Thick peptidoglycan wall retains stain

Gram-

Appears pink when stained with crystal violet

Thin petidoglycan wall therefore poor stain retention

198
Q

Describe the main features of bacteria.

A

Plasmids

Cell envelope

Flagella

Pili

Capsule + slime layers

Endospores

199
Q

What mechanisms of the innate immune system are there to combat bacteria?

A

Acute phase proteins (opsonins)

Complement - alternative pathway

Phagocytosis by neutrophils

Macrophage activation

PAMPs recognised by PRRs

200
Q

What are PAMPs?

A

Conserved molecular motifs on pathogens

e.g. lipopolysaccharides, flageillin

201
Q

What are the mechanisms that recognised PAMPs?

A

Toll-like receptors (TLRs) + PRRs on host cells

202
Q

Describe the role of TLRs.

A

Found on monocytes/macrophages, mast cells + B-cells

Recognise PAMPs on bacteria

Triggering of TLRs → cytokines + inflammation

Capable of some recognition of bacteria, though lack specificity

203
Q

Describe the process of phagocytosis.

A

Macrophages ingest + degrade particulate ag through the use of long pseudopodie that bind + engulf bacteria

Engulfed bacteria are degraded when the phagosome fuses with a vesicle containing proteolytic enzymes ⇒ phagolysosome

204
Q

By what means do bacteria avoid phagocytosis?

A

Bacterial capsule

Protein A - binds IgG, activates C3 → decreases complement

M-protein - blocks complement activation + reduces opsonisation

205
Q

What mechanisms can bacteria utilise to promote their survival within host cells?

A

Infiltrate phagolysozomes

Manipulate host cytokine responses - altering balance of Th1 + Th2

Causes TH2 > TH1

206
Q

What happens to pathogens if TH1 cells are stimulated?

A

TH1 cells direct response to inhibit IC pathogens

TH1 cells secrete IFN-gamma to activate macrophages + Tc cells

207
Q

What happens to pathogens if TH2 is promoted?

A

TH2 suppresses activation of macrophages

TH2 promote strong ab-response based on neutralising IgGs

* most effective to combat EC pathogens

208
Q

Compare the 2 main methods of acquired immunity to bacteria: humoral vs. cell-mediated.

A

Ab-mediated (humoral)

  • neutralises toxins
  • kill bacteria - IC method by macrophages
  • opsonises bacteria
  • essential protection for neonates

Cellular immunity

  • mainly Th1 responses
  • direct killing by Tc + NK cells
209
Q

Give 4 examples of bacteria that hide within hosts cells to avoid the host immune system.

A

Chlamydophila psittaci

Salmonella

Rickettsia

Bartonella

210
Q

By what means can bacterial avoid ab-defences of host?

A

IgA protease which cleaves ab found in mucosal secretions

Antigenic variation - turns pili on/off

Mimic host - look like self-ag

Biofilm formation

211
Q

How can bacteria cause injury to host tissues?

A

Secreted exotoxins

Membrane-bound endotoxins

Non-specific immune stimulation

Specific humoral + CMI stimulation

212
Q

How do bacterial endotoxins cause damage to host tissues?

A
  • can cause food poisoning even in absence of organism
  • immune systems often target toxins with neutralising abs

* whilst endotoxins are susceptible to ab, many are so toxic that they may be fatal to host before defensive ab can be produced

213
Q

Describe the process of endotoxic shock.

A

Excessive release of cytokines can lead to:

  • intravascular coagulation with consequent defective clotting
  • changes in vascular permeability
  • loss of fluid into the tissues
  • fall in BP (risk of hypovolemia)
  • circulatory collapse
  • haemorrhagic necrosis - especially in the gut
  • * may be fatal*
214
Q

How can bacterial endotoxins damage the host organism?

A

Lipopolysaccharide - activates macrophages to release inflammatory cytokines

Lipid A - toxic if organism enters bloodstream → massive immune cell infiltration + activation of coagulation

215
Q

How do superantigens cause damage to host tissues?

A
  • polyclonal T-cell activators
  • produced by bacteria to induce ineffective host immunity
  • hyperstimulate immune system: fever, nausea, D++, V++
  • leads to shock ⇒ organ failure + circulatory collapse

= cause of toxic shock syndrome (TSS)

216
Q

What is the significance of serology with regards to bacterial infections?

A

Detects specific ab to organism - useful for Dx

  • often general increases in serum Igs are seen in conjunction with severe or systemic bacterial infections
217
Q

What are the 2 main classifications for fungi?

A

Moulds - filamentous, spore-forming

Yeasts - unicellular, budding mechanism for reproduction

218
Q

Describe innate immunity of hosts to fungal infections.

A
  • alternative complement pathway is activated
  • phagocytosis is weak → bystander damage is severe due to ‘frustrated’ phagocytosis
219
Q

Describe the process of acquired immunity to fungal infections in hosts.

A
  • once infected, only T-cell responses are effective - mainly by activating local macrophages + promoting tissue repair
  • some Tc responses
  • fungal infections common in animals with defective T-cell immunity
220
Q

What is the significance of macrophages releasing cytokines?

A

This:

  • attracts other cells
  • induces fluid exudate from blood
  • exudate contains complement + other antimicrobial products
221
Q

Describe the basic features of viruses.

A

Small particles that infect cells

Obligate IC parasites - lack reproductive machinery

Threatened by immunity or death of host

222
Q

What different types of virus are there?

A

DNA viruses

RNA viruses

223
Q

What is the infection strategy of viruses within their natural hosts?

A

In natural hosts - there is no disease

224
Q

What tends to happen in 2º virus hosts?

A

Vira infection can be lethal

225
Q

Give 3 examples of DNA viruses.

A

Herpesviridae

Adenoviridae

Parvoviridae

226
Q

Give 6 examples of RNA viruses.

A

Paramyxoviridae

Orthomyxoviridae

Coronoviridae

Picornaviridae

Caliciviridae

Flaviviridae

227
Q

What are the general steps of viral reproduction?

A
  1. Viral invasion of host cell
  2. Synthesis of new viral nucleic acids + proteins
  3. Self-assembly of new viral macromolecules into virus particles
  4. Virus particles released from host cell
228
Q

What are the possible consequences for a cell infected by a virus?

A

Lytic infections = destruction of the host cell caused by virulent viruses

Persistent infections = do no lead to cell lysis, release viral particles slowly over a long period

Latent infections = delay between the infection process + the appearance of symptoms

Transformation = some animal viruses can change a normal cell into a tumour cell

229
Q

What are the problems posed by viruses and treating them?

A

Constantly evolving due to short 1/2 - new forms appear spontaneously

Tx are very restricted or absent

Evolution selects for ‘smart’ viruses

230
Q

What is the role of interferons against viruses?

A

Secreted within hours of infection

231
Q

What different kinds of interferons are there?

A

Type 1 = IFN-a & IFN-ß

  • produced by tissue cells (fibroblasts)
  • stimulate NK activity against viral cells + NK secretion of IFN-gamma

Type 2 = IFN-gamma

  • from activated T + NK cells
  • prevents viral growth in cells by induction of NO secretion + more IC IFN production
  • activates macrophages
232
Q

What are the functions of IFN-a and IFN-ß?

A
  • induce resistance to viral replication in all cells
  • increase MHC I expression + ag presentation in all cells
  • activate NK cells to kill virus-infected cells
233
Q

Which type of cells produce IFN-a + IFN-ß?

A

Virally infected cells

234
Q

What type of interferon is produced by T-lymphocytes responding to ag?

A

IFN-gamma

235
Q

What does ADCC refer to?

A

A mechanism of CMI whereby an effector cell of the immune system actively lyses a target, whose membrane surface-ag have been bound by specific ab.

236
Q

Which cells are responsible for ADCC (ag-dependent cell-mediated cytotoxicity)?

A

FcR+ cells

237
Q

What are the functions of ab-mediated immunity?

A

Blocks absorption of virions to target cells

Stimulates phagocytosis of viruses

Triggers complement-mediated lysis

Triggers ADCC by FcR+ cells

Viral clumping (agglutination)

238
Q

Which of the Igs is most important for ab-mediated immunity?

A

IgG

239
Q

In what ways might ab enhance disease?

A

Mediate virus attachment to some cells e.g. FcR/C3b

Hypersensitivity reactions

240
Q

What kind of cells are targeted by NK cells?

A

Cells whose MHC class I is reduced

241
Q

What is the agent responsible for stimulating NK cell activity?

A

IFN

242
Q

What 2 means are there for eradicating virally infected cells?

A

NK cells

Tc cells

Macrophage elimination

243
Q

What mechanisms do viruses have of evading immune systems?

A

Interfering with IFN

Surviving phagocytosis

Evading ab responses

Inhibiting infected cell death

Inducing immunosuppression

Evading T-lymphocyte responses

Stress can activate latent infections

244
Q

Give 2 conditions that result as adverse consequences of viral immunity.

A

Distemper - demyelination: brain macrophages ingest immune complexes containing distemper which releases toxic products damaging neurones

Canine adenovirus - deposition of immune complexes in cornea + PMN release damaging enzymes → opacity to eye

245
Q

What 3 classes of parasites are there?

A

Protozoa

Worms (helminths)

Arthropods (insects, arachnids)

246
Q

How do parasites damage their hosts?

A

Competing for cell nutrients

Disrupting tissues

Destroying cells

Mechanical blockage

247
Q

How does a direct parasite life cycle work?

A

Same host is reinfected

248
Q

What is the term used to describe infection of different hosts before the original host is re-infected?

A

Indirect life cycle

249
Q

Describe the features of protozoa.

A

Single-celled eukaryotic microorganisms

Lack cell walls

Many possess a cyst that protects from adverse conditions

2 important sub-phyla: Sarcodina + Mastigophora

250
Q

What methods do protozoa have for evading their host’s innate immunity?

A
  • resistance to complement
  • surviving inside phagocytes
  • manipulating dendritic cells
  • poor PAMP expression
251
Q

How does the host respond to parasitic infection?

A
  • ab - control parasites numbers in blood + tissues, driven by TH2
  • CMI - IC parasites controlled by TH1
  • *often both pathways are needed for effective immunity*
252
Q

How effective are vaccinations against protozoal infections?

A
  • limited success
  • frequently requires a cocktail of species/strains for maximising vaccination success
253
Q

What is the main problems that helminth infections present to their host immune system?

A

Most are EC + too large for phagocytosis

254
Q

What is the main mechanism used to target helminth infections?

A

TH2 response - very strong

  • release of inflammatory mediators
  • high levels of IL-4, IgE, many eosinophils + mast cells at infection sites
  • ag-bound IgE attach to their specific IgE FcR on mast cells → degranulation
255
Q

How do eosinophils respond to parasite infection of the host?

A

IgE binds to worm

Binding of FcR to IgE triggers activation ⇒ release toxic mediators

→ breakdown of worm’s cuticle

256
Q

How is the TH2 response selected in favour of TH1 mechanism?

A

IL-4 driven

257
Q

Describe the process of TH2 in eliminating parasite infections within a host.

A

TH2 cells suppress macrophage activation; stimulating eosinophils + mast cell action

Generates a strong ab response based on neutralising IgE + IgG

  • best method for combatting EX pathogens
258
Q

What are the roles of eosinophils + mast cells in parasite infection?

A

Mast cells stimulate worm expulsion

Eosinophils kill worms

259
Q

How does CMI respond to helminth infection?

A

Some Tc responses

Sensitised T-lymphocytes attack by:

  • macrophage attraction + activation
  • Tc cells attack larvae
260
Q

What physiological host changes are induced by anti-worm immunity?

A

Increases no. of goblet cells

Increased mucin secretion

Increased intestinal mobility

Increased H2O influx into intestinal lumen

261
Q

By what means can helminths evade vertebrate host immunity?

A
  • size
  • thick extracellular coat
  • adsorbing host proteins
  • anatomical seclusion
  • molecular mimicry
  • surface ag-shedding
  • interference with ag-presentation
  • immunosuppression
  • anti-immunity mechanisms
  • migration
  • production of enzymes
262
Q

How successful are vaccinations against helminth infections?

A
  • poor host immmunity means very few effective vaccines
  • drug Tx are much more common
263
Q

What possible effects can saliva of arthropods have on hosts?

A

Stimulation of TH1

Induction of basophilic infiltration

TH2 response?

Impaired APC ability

264
Q

What agent can parasites release to interfere with immune responses?

A

Free ag

265
Q

What effects does the release of free ag by parasites have on parasites?

A
  1. Block ab
  2. Blockade effector cells
  3. Induce B- + T-lymphocyte tolerance
  4. Induce polyclonal activation to divert immune system
  5. Inhibit the inflammatory response
266
Q

What does polyclonal activation refer to?

A

Activation of B-cells to produce ab specific to epitope identified in response to detection of an ag

267
Q

Describe the main features of cancer.

A

Damaged cells of body that no longer undergo programmed cell death

Growth is no longer controlled

Metabolism is altered

268
Q

Describe the basic features of a tumour.

A

A swelling or lesions formed by an abnormal growth of cells

Might not be due to cancer

A cancerous tumour arises from a single cell proliferating uncontrollably

269
Q

Suggest some potential causes of tumours.

A

Oncogenes

Tumour suppression genes becoming dysregulated

Carcinogens

Age

Genetic make-up

Diet

Immune deficiency

Environment - e.g. plant products

Infections - especially viruses

270
Q

What is the definition of an oncogene?

A

Protein-encoding genes that trigger onset + development of cancer if they dysregulate

271
Q

What different types of tumour are there?

A

Benign

Malignant → metastases

Premalignant

272
Q

What potential mechanisms of the immune system could target tumour cells?

A

Macrophage activity

Dendritic cells - APC

CD8 cell-mediated cytotoxicity

NK activity

ADCC (ab-dependent cell-mediated cytoxicity)

273
Q

What does FcR refer to?

A

Refers to fragment crystallisable receptors found on ab coating pathogens detected by the immune system

274
Q

What different kinds of ag are expressed on tumour cells?

A

Tissue-specific ag

Reactivated gene products

Viral ag

Mutated gene products

275
Q

What are the 3 major cell types involved with tumour immunity?

A

NK cells

Macrophages

CD8 cytotoxic T-lymphocytes

276
Q

Descrive the T-cell mediated response to detected tumour cells.

A

Tumours express ag

Tumour cells phagocytosed by APC (macrophages)

APC expresses ag → triggers TH1 + Tc cells

Tc cells kill tumour

277
Q

By what means can NK cells kill tumour cells?

A

Targeting tumour cells lacking in MHC-I

Kill tumours using ADCC

278
Q

What 2 cytokines are needed to stimulate NK cell growth?

A

IL-2

IFN-gamma

279
Q

What role do IL-2 + IL-4 have within the immune system?

A

Increase cytotoxic T-lymphocyte activity

280
Q

What does TNF refer to?

A

Tumour necrosis factors are cytokines that can causes apoptosis

281
Q

What role do TNF + IL-12 have within the immune system?

A

Induce IFN-gamma secretion by NK cells

282
Q

What mechanisms do tumours have for escaping the patient’s immune system?

A
  • low immunogenicity
  • ag modulation
  • suppression of anti-tumour immune response by tumour cells or T-regulatory cells
  • induction of lymphocyte apoptosis
283
Q

What means are there for treating lymphomas?

A

Chemotherapy - highly effective

Vaccination

284
Q

What is the definition of immunological tolerance?

A

A state of unresponsivenes to a particular ag

285
Q

What is another term describing self-ag?

A

Autoantigen

286
Q

Describe the 5 main mechanisms of post-thymic tolerance.

A
  • self-reactive T cells ignore self-ag + sequestered ones
  • self-reactive T cells abort
  • self-reactive T cells rendered anergic
  • self-reactive T cells deleted
  • maintained by immune regulation ie. TH1/TH2/Treg
287
Q

Describe the features of B-cell tolerance.

A
  • self-reactive B cells removed in bone marrow + spleen
  • self-reactive B cells may abort, be deleted or anergised
  • some self-reactive B-cells will survive + enter circulation
  • lack of T-cells helps prevent B-cell reactivity
288
Q

What 2 kinds of immunological tolerance are there?

A

Central - in thymus + bone marrow

Peripheral

289
Q

What is autoimmunity?

A

Loss of self/non-self discrimination within the immune system, resulting in immune responses + damage to host tissues

290
Q

How does autoimmunity arise?

A
  • exposure of hidden ag
  • formation of new epitopes
  • cross-reactivity with microorganisms
  • induction by viruses
  • immunoregulation deficiency
  • histocompatibility ag
291
Q

What happens in myaesthenia gravis?

A

Autoantibodies are prodced against Ach receptor → prevents muscle from responding to Ach

⇒ muscle wastage

292
Q

How many different types of hypersensitivities are there?

A

4 types

293
Q

What is atopy?

A

The genetic tendency to develop allergic diseases

  • typically associated with heightened immune responses to common allergens
294
Q

What is the normal Ig production process?

A

IgM production within 1º response

Switches to IgG/A production in 2º response

295
Q

Describe type I hypersensitivity.

A

Mast cell degranulation occurs

  • acute anaphylaxis: horse, pig cat - emphysema + intestinal haemorrhage + D++

dog - collapse of hepatic veins

  • specific allergic conditions:
  • urticaria
  • milk or food allergy
  • allergic inhalant dermatitis
  • allergies to drugs, vaccines
  • parasitic allergies
296
Q

Which type of hypersensitivity is associated with frustrated phagocytosis?

A

Type II hypersensitivity

297
Q

Describe the main features of type II hypersensitivity.

A

Damage results from ADCC by NK cells

cytotoxicity due to complement

⇒ ab + complement react to host cells/tissues

* tissue damage is caused by frustrated phagocytosis

298
Q

What condition is an example of type III hypersensitivity affecting the renal system?

A

Glomerulonephritis

299
Q

Describe the process of type III hypersensitivity.

A

Immune complex mediated - form/deposited on host tissues

  • ag-ab complex deposits on endothelium of vessel
  • inflammatory sites localise to area, stimulated by cytokines
  • complement + neutrophils attack ag-ab complex, whilst fibrinous necrosis of endothelium occurs
300
Q

What kind of cells mediate type IV hypersensitivity?

A

T-lymphocytes

301
Q

What molecules are NOT involved in type IV hypersenstivity?

A

Antibodies

302
Q

Describe the process of type IV hypersensitivity.

A

Primed T-cells respond to chronic ag load by production of cytokines

  • cytokines attract + activate macrophages
  • macrophages damage tissues by release of proteolytic enzymes
303
Q

What term is used to describe an ineffective immune response?

A

Immunodeficiency

304
Q

What cells are responsible for rejection of transplants within a recipient body? Why is this?

A

Tc cells + macrophages

Differences in MHC-I + MHC-II in donor + recipient bodies

305
Q

How many different kinds of immunodeficency are there?

A

1º - inherited defects

2º - extrinsic causes

306
Q

What risks are increased in associated with immunodeficiency?

A

Increased susceptiblity to opportunistic infections

Increased risk of tumours

307
Q

Give an example of an inherited deficiency.

A

Complement deficiency - Brittany Spaniels + Finnish Landrace lambs

  • C3 deficiency
308
Q

When are autosomal recessieve genetic disorders presented?

A

Problem allele is only effective when expressed in homologous manner ie. 100% offspring

When heterozygous at 50%, animal is not ill but a carrier

309
Q

What are BLAD + CLAD? And what autosomal recessive condition do they both refer to?

A

Canine leucocyte adhesion deficiency - Irish Setters

Bovine leucocyte adhesion deficiency - Holstein cattle

  • phagocyte deficiency caused by failure of granulocytes to leave blood + enter sites of infection
310
Q

Describe the process of normal inflammation.

A
  • cells migrate from circulation into sites of infection/inflammation to phagocytose bacteria - are attracted by several mediators
  • enabled by increased expression of adhesion molecules selectins on vascular endothelia + integrins on leucocytes by cytokines
  • PMN express CD11b/18 which binds to ICAM-1 on vascular endothelia to enable passage into tissues to deal with infection
311
Q

What is the problem occurring with leucocyte adhesion deficiency (LAD)?

A

Absence of integrin CD11b/18 means no PMN adherence to blood vessel wall → inability to leave circulation + localise at infection sites

  • infection overwhelms animal
  • very high leucocytosis because PMN fail to emigrate into tissues
  • caused by gene mutations, failing to produce CD11b/18
312
Q

Describe the condition of SCID (severe combined immunodeficiency).

A

Seen in the Arab horse

No functional T or B-lymphocytes in circulation or tissues

Foals sicken after MDAs wane (agammaglobulinaemiac)

Autosomal recessive condition

Overwhelming infections → death at 4-6mo

313
Q

What other forms of SCID are there?

A

X-linked (sex-linked) immunodeficiency in Bassett hounds + Corgis

  • thymus has low number of lymphocytes ⇒ low T-cell numbers in circulation, no IgG or IgA, but normal IgM
  • because X-linked, females are carriers only + disease is only seen in males

Jack Russell Terrier SCID

  • autosomal recessive loss of DNA protein kinase leads to faulty recombination of ag-receptors ⇒ non-functional B & T cells, no Igs
314
Q

What is foal immunodeficiency syndrome?

A

Autosomal recessive fatal genetic disease seen in Dales + Fell ponies

B-cell deficiency causes very low Igs

Foals die after loss of MDA - no survivors

Opportunistic pathogens are lethal

  • carrier test is now available
315
Q

Name 3 primary autosomal recessive defective conditions.

A

Genetic IgM deficiency in Arab/quarter horse foals

Thymic aplasia in nude cats - T-cell deficiency

Ehlers-Danlos syndrome - fragile hyperextendable skin + immunodeficiencies

316
Q

Name 7 potential causes of 2º immunological defects.

A
  1. Viruses
  2. Microbial/parasite infections
  3. Toxins
  4. Malnutrition
  5. Exercise
  6. Trauma
  7. Age
317
Q

Desribe the main features of retroviruses.

A

Affect primary or secondary lymphoid tissues

Phospholipid envelope

RNA

Reverse transcriptase enzyme

318
Q

Give 4 examples of small animal immunodeficiencies.

A

Feline immunodeficiency virus (FIV)

Feline leukaemia virus (FeLV)

Canine distemper virus

Canine parvovirus

319
Q

Give 4 examples of canine infectious immunodeficiencies.

A
  • Ehrlichiosis
  • Anaplamosis
  • Leishmaniasis
  • Demodicosis
320
Q

What are the main immunological tests used for?

A

Infections

Hypersensitivities

Autoimmunity

Immune function

321
Q

What does serology test for?

A

Detection of specific ab to indicate the presence of a specific infection

322
Q

What is the result of clonal selection + expansion of B cells?

A

Generates plasma cells + memory cells

323
Q

What can be done to distinguish between infected and vaccinated animals?

A

Modify vaccine given to include extra (marker) ag targets

  • requires extra serological test, but specificity is assured
324
Q

What different forms of serological test are there?

A

Double immunodiffusion assays

Radial diffusion assays

Bacterial agglutination

Immunoelectrophoresis

RBC agglutination

325
Q

Describe the process of double immunodiffusion assays.

A

ag + ab are placed in wells cut into agar gel and allowed to migrate towards each other

  • a line of precipitation may be formed where the 2 reactants meet
  • if the ag +/- ab wells contain several molecular species then multiple lines of precipitation are possible
326
Q

What are the 3 basic patterns of precipitation possible from double immunodiffusion?

A

Lines of identity

Lines of non-identity

Lines of partial identity

327
Q

How does a single radial immunodiffusion (SRID) assay work?

A

As the ag diffuses radially a ring of precipitation forms around the well + moves outwards

Eventually becomes stationary at equivalence point

328
Q

What is immunoelectrophoresis used for?

A

Detecting B-lymphocytes myelomas

329
Q

How does electrophoresis work?

A

Allows serum proteins to be separated by an electrical current

330
Q

Describe the process of immunoelectrophoresis.

A

Patient’s sera are separated by electrophoretic mobility

Then ag are detected by specific ab

331
Q

What is myeloma?

A

Unrestricted multiplication of one plasma cell secreting one particular Ig

332
Q

How would myeloma be detected?

A

Using immunoelectrophoresis (IEP)

  • unrestricted multiplication of one plasma cell secreting a particular Ig → increase in serum conc of specific Ig
  • therefore a myeloma would show a particularly thick heavy chain with corresponding thick light chain

* an increase in a heavy chain without specific light chain increase will be polyclonal + probably due to infection/inflammation

333
Q

How would polyclonal stimulation be detected in IEP?

A

All Igs levels would be raised in excess

334
Q

How would immunosuppression be determined by IEP?

A

All Ig levels would be within a state of deficiency

335
Q

How are positive + negative RBC agglutination results detected?

A

Positive result: RBC agglutination occurs within test tube

Negative result: RBC settle as ‘button’ within test tube

336
Q

What different agglutination methods are there?

A

Bacterial

Viral

RBC

Particles coated with ag - RBC; latex particles

337
Q

What methods can be used to label abs?

A
  • fluorescent tags
  • enzyme tags
  • gold particles
  • radioisotopes
338
Q

What are the main features + advantages to using an ELISA? What does ELISA stand for?

A

Enzyme-linked immunosorbent assays

  • quantifiable
  • quick
  • reproducible
  • inexpensive
  • doesn’t require complex training to use
  • can detect ag + ab
339
Q

How do non-agglutination tests function?

A

Rely upon having reagents to detect host ab responses

  • ab for detecting IgG, IgA + IgM will need to be tagged with a label for subsequent detection
340
Q

How does immunofluorescence work? What different kinds of immunofluorescence are there?

A

Uses commercial ab tagged with a fluorescent molecule

e.g. FITC, rhodamine

Fluorescence is observed using UV microscope

Direct vs. indirect methods

341
Q

How do the different methods of immunofluorescence compare?

A

Direct: detects ag in tissues

Indirect: detects ab in sera

342
Q

How does a complement fixation test work?

A

Immune complexes bind + consume complement

Therefore depletion means no remaining complement to lyse ab-coated RBCs

343
Q

What is the alternative name for immunoperoxidase staining? How does this method work?

A

Horse radish peroxidase

Uses wax sections

Uses LM

Good tissue architecture

Counterstaining possible

Good morphology

Coloured targets for better visibility

344
Q

What 2 kinds of neutralising tests are there?

A

Virus neutralisation tests

Haemagglutination inhibition test

345
Q

Which type of hypersensitivity is TB-testing based on?

A

Type IV hypersensitivity - mediated by T-lymphocytes

346
Q

How does flow cytometry work for immunological testing?

A

Identifies cell surface markers - e.g. T + B-lymphocytes

Cells incubated with markers are tagged with fluorescent probes

Cells are passed through laser beam which detects different coloured cells ⇒ marker profile

Pathology (7 decks)

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