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Blood, Immunity and Infection > Immunity > Flashcards

Immunity Flashcards

1
Q

3 things that promote phagocytosis

A

Common bacterial cell wall components (PAMPs)
C3b complement component
Fc region of antibodies

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2
Q

3 types of PAMPs

A

Common cell wall structures e.g., LPS and peptidoglycans
Bacterial metabolic processes
Heat-shock proteins (released by stressed cells)

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3
Q

Acute phase proteins

A

Produced early in infections and tissue injury in response to early alarm mediators
Act to enhance host resistance, minimise tissue injury and promote resolution and repair of inflammatory lesions

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4
Q

Effector cells

A

B cells
CD8 cells
Natural Killer cells

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5
Q

Regulator cells

A

CD4 cells

Th1, Th2, Treg + T17

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6
Q 
Specialised APCs of the:
Skin
Lungs
Blood
Liver
Gut
A

Skin – Langerhans cells (transport to regional nodes)
Lungs – Alveolar macrophages (transport to spleen or regional nodes)
Blood – Blood monocytes (transport to spleen)
Liver – Kupffer cells (transport to spleen or regional nodes)
Gut – Epithelial M cells (transport to Peyer’s patches)

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7
Q

Process of antigen presentation by APC e.g., skin wound

A

Multiplying bacteria uptaken into Langerhans cells of skin
Dendritic cells bind bacteria and transport it through lymphatics
Antigen enters lymph node, followed by small naive lymphocytes from the bloodstream
T cells migrate to paracortical areas of nodes and B cells migrate to follicles
Lymphocytes that recognise the antigen are activated and stop recirculating
Lymphocytes that do not recognise the antigen leave via afferent lymphatic vessels
After several days activated lymphocytes leave the efferent lymphatic vessel as effectors
Meanwhile, antigen is held in lymph node and antigen-specific cells are recruited

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8
Q

Endogenous pathway of antigen processing

A 
Used for peptides derived from cytoplasmic proteins, like in viral infections
Cytosolic proteins degraded into peptide fragments by proteasomes
Peptides produced are unaccessible to class I MHC molecules, which are bound to the TAP-1 transporter complex on the ER membrane
Peptides transported into ER lumen by TAP-1 transporter and inspected by TAP-1-bound class I MHC
When a peptide binds to class I MHC, the MHC molecule folds around the peptide and is released from TAP-1 to be transported to the cell membrane
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9
Q

Exogenous pathway of antigen processing

A 
Used for peptides derived from ingested material
Antigen is taken up from outside the APC into intracellular vesicles
Acidification of vesicles activates proteases to degrade antigen into peptide fragments
Vesicles containing peptide fragments fuse with vesicles containing class II MHC and peptides with affinity for antigen-binding groove of class II MHC bind to it
Bound peptide transported by class II MHC to cell surface
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10
Q

Where are class I MHC molecules expressed?

A

Virtually all nucleated cells in the body
Therefore most cells can present peptide fragments derived from metabolic breakdown of intracellular infectious processes

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11
Q

Where are class II MHC molecules expressed?

A

Only on B cells and professional APCs

Therefore only these cells can present peptide fragments of ingested material

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12
Q

Th1 cells have activity against:

A

Viruses, bacteria and intracellular agents

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13
Q

Th2 cells have activity against:

A

Parasites, allergies and multicellular agents

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14
Q

The main role of Treg cells is to:

A

Downregulate other responses/suppress antigen-specific

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15
Q

The main role of Th17 cells is:

A

Inflammation and mucosa maintenance

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16
Q

4 types of immune conversations

A

Adhesion molecules
Co-stimulator molecules
Cytokines
Hormones

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17
Q

3 types of adhesion molecules

A

Selectins
Integrins
Cadherins

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18
Q

Co-stimulators

A

Surface molecules induced on antigen-presenting cells and lymphocytes
Involved in modulating lymphocyte activation and function

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19
Q

Example of co-stimulators found on B cells

A

CD40 (which binds to CD40-L on CD4 T cell)

CD40 then upregulates B7 which binds CD28 on the T cell which then releases cytokines

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20
Q

Type I interferons

A

IFN-a and IFN-B

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21
Q

Proinflammatory cytokines

A

IL-1, IL-6 and TNF-a

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22
Q

Adaptive immune response cytokines

A

Il-1, Il-2, IFN-y and IL-4–6

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23
Q

Chemokines

A

IL-8, MCP-1 and MIP-1a

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24
Q

Haematopoietic cytokines

A

IL-3, G-CSF, M-CSF, GM-CSF, IL-5 and IL-7

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25
Q

IL-1

A

Second messenger to activate T cells following contact with antigen

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26
Q

IL-2

A

Stimulates clonal proliferation of antigen-specific T cells

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27
Q

IFN-y

A

Causes activation of macrophages, promotes HLA expression and activates NK cells

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28
Q

IL4–6

A

Important in stimulating growth and differentiation of B cells

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29
Q

IL-8

A

Influences neutrophil chemotaxis and activation

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30
Q

CSF cytokines

A

Stimulate proliferation of granulocytes (G) and monocytes (M)

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31
Q

IL-3

A

Promotes proliferation of all lineages of haematopoietic cells

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32
Q

IL-5

A

Stimulates eosinophil growth and activation. Also important in allergic responses

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33
Q

IL-7

A

Stimulates erythroblast and megakaryocyte growth and involved in B cell development

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34
Q

MCP-1 and MIP-1a chemokines

A

Important in allergic inflammation by stimulating basophils to release histamine

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35
Q

Adhesion molecules

A

Link cells to other cells
Important in binding lymphocytes to antigen-presenting cells and also in directing lymphocytes and phagocytic cells to parts of the body where they are needed

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36
Q

Co-stimulator molecules

A

Pass signals between linked cells through surface–surface interactions to trigger or inhibit antigen-specific effects

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37
Q

Cytokines

A

Soluble glycoproteins that signal cells expressing specific cytokine receptors e.g., lymphocytes following antigen activation

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38
Q

Hormones

A

Soluble molecules produced by neuroendocrine hormones that modulate the response of antigen-activated cells

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39
Q

3 types of selectins

A

L-selectin (lymphocytes)
P-selectin (platelets)
E-selectin (endothelial cells)

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40
Q

Integrins

A

Important in cell–cell adhesion and cell–ECM adhesion

Hold lymphocytes together for activation and hold lymphocytes on capillary wall

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41
Q

Leukocyte adhesion deficiency

A

Hereditary deficiency of some integrins

Leukocyte trafficking impaired and patients are susceptible to recurrent pyogenic infections

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42
Q

Anergy

A

Fail-safe mechanism that prevents T cells from responding to self-antigens
Occurs when an antigen is presented to a T helper cell without the required co-stimulator molecule being presented on the APC causing the T cell to become paralysed

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43
Q

Properties of IgM

A

Large pentamer, confined to bloodstream, does not cross placenta, 3rd most common
Produced early in primary antibody response, good defence against bacterial spread
Efficient agglutinator and complement activator

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44
Q

Properties of IgG

A 
Small monomer, diffuses easily out of blood, crosses placenta, by far the most common
Major class in secondary responses
Good complement activator, opsonin and Fc receptor-mediated effector mechanisms
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45
Q

Properties of IgA

A

Defends exterior surfaces

2nd most common

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46
Q

Properties of IgD

A

Trace amounts
HIghly sensitive to proteolysis
Receptor on virgin, antigen-sensisitve B lymphocytes

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47
Q

Properties of IgE

A

Trace amounts unless allergy or parasite infection

High affinity Fc receptor on mast cells and basophils

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48
Q

Antibody structure

A 
Four polypeptide chains held together by disulphide bonds and non-covalent interactions
Light chains and either kappa or lambda
Heavy chains can be one of 5 types with each giving rise to the class of antibody
Variable and constant regions on the top of the Y
Also an Fc region on the bottom of the Y containing the bottoms of the heavy chains, which are constant regions, a complement-binding region and a hinge region
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49
Q

Antibody class switching

A

IgM is the first class of antibodies to be synthesised in a primary antibody response
After some time, IgM synthesis begins to decrease and is replaced by IgG production
Individual activated B cell clones begin by producing IgM, but then switch to IgG
IgG synthesis is dramatically increased in secondary responses because memory cells preferable make IgG over IgM. IgM mostly due to activation of new naive antigen-sensitive B cells seeded to secondary organs from bones marrow after initial antigen contact

50
Q

Properties of antibodies

A 
Direct neutralisation
Agglutination
Opsonisation
Antibody-dependent cell-mediated cytotoxicity
Activation of complement cascade
51
Q

Direct neutralisation

A

Blocks attachment and entry to host cells by physically preventing adsorption of viral/bacterial particles
Immobilises bacterial flagella

52
Q

Agglutination

A

Antibodies clump small particles into larger complexes which are easier to ingest and phagocytose
However, too much can be dangerous – agglutination must be moderated

53
Q

Opsonisation

A

Granulocytes and macrophages have surface receptors for the Fc region of Igs and C3b. Phagocytes can bind these cells using antigen–antibody complexes with high affinity to enhance phagocytosis.

54
Q

Antibody-dependent cell-mediated cytotoxicity

A

NK cells have Fc and C3b receptors on their surface
Not phagocytic but kill cell material that they bind to through antibody or C3b mediators by delivering short-range cytotoxicity factors

55
Q

Properties of C3a

A

Anaphylotoxin i..e, stimulate mast cells to release histamine which causes increased vascular permeability and vasodilation
Chemotaxis

56
Q

Properties of C3b

A

Opsonisatation
Very reactive and has a short half-life
Binds C3 convertase to make C5 convertase

57
Q

Properties of C5a

A

Chemotaxis

58
Q

Properties of C5b

A

Makes up part of the complex membrane attack system

59
Q

Autologous

A

Donor tissue from recipient

60
Q

Syngeneic

A

Genetically identical donor and recipient

61
Q

Allogeneic

A

Genetically non-identical donor and recipient from same species

62
Q

Xenogeneic

A

Donor species different from recipient

63
Q

B cell ontogeny and self-tolerance

A

B cells mature in bone marrow through pre-B cell stage where only the heavy chain is rearranged, and immature B cell stage where both heavy and light chains are rearranged
This produces sIgM and sIgD
Potentially self-reactive B cells censored at immature B cell stage
Mature B cells can switch Ig classes while retaining same antigen-binding specificity

64
Q

T cell ontogeny and TCR genes

A

Undergo rearrangement during T cell development
T cells develop in thymus from immature stem cells into mature, antigen-sensitive T cells by TCR gene rearrangement, positive selection for self-MHC recognition, negative selection to eliminate strongly auto-reactive cells, and CD4/CD8 differentiation

65
Q

Sources of diversity in B and T cell repertoires

A

Multiple V, D and J exon segments
Combinatorial diversity among exons
Base substitutions at V-J and V-D-J joining boundaries
Somatic mutations within hypervariable regions

66
Q

Adoptive transfer

A

Transfer of immunity from one animal to another by transfer of cells or antibodies
Can result in graft rejection due to T lymphocyte activity mostly

67
Q

Cytotoxic T cell activation

A 
Secondary lymphoid organs contain cytotoxic T cell precursors: antigen-sensitive CD8 T cells, which each have a set of TCRaB receptors
Foreign antigens come into contact with these precursors
T cells with TCR receptors that bind most strongly to the antigen presented by class I MHC are selected and activated via signal 1
Further activation signals provided by costimulator interactions and cytokines from TH cells
Cytotoxic precursors proliferate and differentiate into cytotoxic effector cells and the memory population
68
Q

Cross-priming

A 
CD8 T cells recognise antigens presented by class I MHC (endogenous pathway) but also require activation signals from CD4 helper T cells, which recognise antigens presented by class II MHC (exogenous pathway)
Therefore dendritic cells present exogenous antigens to CD4 cells and receive signals back from these activated helper cells to license the dendritic cells to present some exogenously-acquired antigens through the endogenous class I MHC pathway to present to CD8 cells to activate them
69
Q

3 mechanism through which cytotoxic T cells kill their targets

A

Insert perforin into the target cell membrane which assemble into donut-shaped holes in the membrane
Release enzymes that digest the membrane
Release cytokines that bind to receptors on target cells to induce apoptosis

70
Q

Ig gene rearrangement process in bone marrow

A

1) Heavy chain rearrangement at pre-B cell stage (V–D–J)
2) Light chain rearrangement (kappa then lambda if kappa rearrangement fails)
3) Splicing
4) Expression of surface IgM (immature B cell)
5) Test for sIgM receptor binding to self-antigens in the bone marrow
6) If no self-recognition then expression of surface IgD and export to secondary lymphoid organs (mature B cell)

71
Q

Central tolerance

A

Some receptors may be able to recognise self-antigens due to random, antigen-independent Ig gene rearrangement, therefore immature B cell receptors are tested for self-antigen binding in the bone marrow. If the receptors bind with high infinity, the cell is deleted.

72
Q

TCR gene rearrangement in the thymus

A

1) Heavy chain (B or y) rearrangement (V–D–J–C)
2) Light chain (a or d) rearrangement (V–J–C)
3) Splicing

73
Q

Where are TCRyd-bearing cells found?

A

Mostly in the mucosa of the gut and the skin
May play a role in early defence against pathogens – known to respond to heat shock proteins expressed by invading micro-organisms in response to stress

74
Q

T cell positive selection

A

Recognition of self-MHC – if T cell responds, it survives

75
Q

T cell negative selection

A

T cells that respond to self-MHC PLUS self-peptide so strongly that they are self-reactive in the absence of foreign antigen are killed

76
Q

Double positive CD4/CD8 T cells

A

Cortical thymocytes express both receptors before they down-regulate one to be single positive via differentiation
Positive selection occurs when they are double positive, negative selection occurs after T cells become single positive

77
Q

4 factors relating to the micro-organism regarding infection

A

Type of micro-organism
Degree of exposure
Virulence
Route of entry

78
Q

5 factors relating to the host regarding infection

A 
Integrity of non-specific defences
Competence of specific immune system
Genetic capacity to respond normally to a specific organism
Evidence of previous exposure
Co-infection
79
Q

6 specific immune factors regarding infection

A 
Direct neutralisation by antibodies
Opsonisation and phagocytosis
Complement-mediated effects
T cell cytotoxicity
Inflammatory and immunoregulatory cytokines
Anti-viral cytokines (interferons)
80
Q

2 reasons that antibodies are important in infection

A

Recovery from extracellular infection

Protection of mucosal surfaces

81
Q

Antibodies active against virus particles

A

A, G and M

82
Q

Antibodies active against toxins

A

G and M

83
Q

Antibodies active against extracellular bacteria

A

A, G and M

84
Q

Antibodies active against parasites

A

E and M

85
Q

Describe antibody concentrations across the life-span

A

In utero, maternal IgG is present from 3 months, increasing rapidly until birth.
After birth, maternal IgG decreases rapidly, levelling off around 2–3 months. Completely disappears by 8 months
Baby’s own IgG begins to be made after one month and shoots up. More prominent than maternal IgG at 2 months and levels off at 3 months, but continues to increase. 80% of adult IgG levels at 12 months.
IgM starts to be produced at 7 months in utero, but is slow and gradual. At 12 months after birth, IgM at 75% adult levels.
IgA starts to be produced at 2–3 months after birth, but is slow and gradual. At 12 months after birth, IgA at 20% adult levels. IgA also passed through breast milk.

86
Q

What are cytotoxic T cells effective against?

A

Viruses (cytoplasmic peptides), tumours and transplanted organs

87
Q

Surface IgA

A

IgA gives protection in external body fluids, tears, saliva, nasal secretions, and intestine/lung surface fluids
If an infectious agent penetrates the IgA barrier, it will come up against the IgE facet of the secretory system (mast cells)

88
Q

NK cells key points

A

Large, granular leukocytes in the blood, spleen and peritoneal exudate
Identified by presence of CD16 Fcy receptor and CD56 surface marker
Do not have rearranged Ig (like B cells) or TCR (like T cell) genes
Activated to kill cells that have down-regulated class I MHC expression – these cells are often virus-infected or tumour cells
Activity can be enhanced by CD4 T cell-produced cytokines

89
Q

Role of CD16 receptor in NK cells

A

Bind antibodies attached to target cells and exhibit antibody-dependent cell-mediated cytotoxicity

90
Q

What determines viral infection recovery?

A

Cytotoxic T cells and IFNs, rather than antibodies

91
Q

Antibodies associated with Th1 CD4 T cells

A

IgM and IgG

virus and acute bacterial infections

92
Q

Antibodies associated with Th2 CD4 T cells

A

IgG and IgE

chronic infections, especially parasites

93
Q

Balance of Treg and Th cells

A

The balance between the four subsets of CD4 T cells has evolved due to a diverse variety of antigens that humans have been exposed to. Due to a revolution in technology and cleanliness, humans are exposed to much fewer antigens and barely any parasites. As a consequence of this, without the time to evolve and recalibrate the balance of these different subpopulations, it seems that Th17 cells, which are now more used in an age where inflammatory diseases are much more common than parasitic infections, are massively upregulated, bringing with it a new wave of autoimmunity and allergies.

94
Q

4 types of hypersensitivity

A

Type I IgE: IgE-mediated/allergic/anaphylactic
Type II IgG: Antibody-mediated/cytotoxic
Type III IgG: Immune complex-mediated
Type IV Th cells: T cell-mediated/delayed-type hypersensitivity

95
Q

Type I hypersensitivity

A

Occurs when a divalent allergen cross-links two IgE molecules which were previously passively bound to high affinity Fce receptors. Mast cell mediators are released.

96
Q

2 types of mast cell mediators

A

1) Granule-associated performed mediators

2) Newly formed mediators

97
Q

Examples of granule-associated mediators

A

Histamine
Heparin
Enzymes
Chemotactic and activating factors e.g., eosinophil chemotactic factor, neutrophil chemotactic factor, platelet activating factor

98
Q

Examples of newly formed mediators

A

Lipoxygenase pathway products e.g., leukotrienes

Cyclooxygenase pathway products e.g., prostaglandins, thromboxanes

99
Q

Main effects of mediators released in type I hypersensitivity

A

Vasodilation
Vascular leakiness
Pruritis
Smooth muscle contraction

100
Q

Treatment of Type I hypersensitivity

A 
Avoidance
Antihistamines
Corticosteroids
Sodium cromoglycase
Sympathomimetics e.g., epi-pen
Desensitisation
101
Q

Desensitisation

A

Theory revolves around slowly exposing a person to their allergen in the hopes of replacing the IgE binding to the Fce receptors with IgG binding, which does not produce an allergic reaction

102
Q

Atopic patients

A

Patients with a tendency to make IgE antibodies to multiple allergens

103
Q

Bronchial reactions to allergens

A

Immediate phase due to IgE reaction late phase due to IgG reaction

104
Q

Type II hypersensitivity

A

Mediated by IgG targeting membrane-associated antigens. Involves a sensitization phase leading to antibody production to recognize substances or metabolites that accumulate in cellular membrane structures. In the effector phase, target cells become coated with antibodies (opsonisation) which leads to cellular destruction by frustrated phagocytosis, complement-dependent cytotoxicity and ADCC.

105
Q

Frustrated phagocytosis

A

Phagocyte unable to engulf whole target, therefore releases vacuole contents to break it down into smaller parts ready for ingestion. When this happens in type II hypersensitivity, it damages host cells too.

106
Q

Type II hypersensitivity: Frustrated phagocytosis

A

IgG coat target cells and bind to Fc receptors present on cells such as macrophages and neutrophils and mediate phagocytosis and activate complement via the classical pathway. This leads to C3b deposition which mediates phagocytosis.

107
Q

Type II hypersensitivity: CDC

A

Complement activation leads to production of the MAC, which forms pores in the cellular membrane resulting in cytolysis (complement-dependent cytotoxicity).

108
Q

Type II hypersensitivity: ADCC

A

IgG antibodies bind NK cells and macrophages and cause granzyme and perforin release resulting in cell death by apoptosis (ADCC).

109
Q

Type III hypersensitivity

A

Binding of antigen and complementary antigen and recruitment of other inflammatory cells by soluble mediators. Large immune complexes are formed by cross-linking and get lodged in small vessels, activating immune processes and damaging the vessels. Can be systemic or localised.

110
Q

Systemic type III hypersensitivity

A

Complexes deposit around the body, commonly the skin, resulting in a rash, the joints, resulting in arthritis and the kidneys, resulting in nephritis. Common example is serum sickness and non-human monoclonal antibodies.

111
Q

Localised type III hypersensitivity

A

Occurs in tissues. IgG antibodies from the circulation meet antigens and activate complement and recruit inflammatory cells. Common example if Farmer’s lung, where actinomycete fungi grow in hay and are inhaled, causing extrinsic allergic alveolitis.

112
Q

Type IV hypersensitivity

A 
Initial phase involves uptake, processing and presentation by dendritic cells in the skin and then presentation of antigen to T cells in nearby lymph nodes
T cells (mainly Th1) secrete cytokines to recruit and activate macrophages. Also causes upregulation of adhesion molecules and MHC expression on keratinocytes.
Normal proteins act as carriers for small molecules, which are transported to lymph nodes, causing T cell stimulation. Then memory Th1 cells return to the site and provoke inflammation.
113
Q

Mantoux reaction

A

Classic example of type IV hypersensitivity which is utilised to test for memory against Tb antigens

114
Q

4 mechanisms of tolerance

A

Clonal deletion
Clonal anergy
Immunological ignorance
Suppression

115
Q

Clonal deletion

A

AKA central tolerance

Complete removal of self-reacting cells

116
Q

Clonal anergy

A

AKA peripheral tolerance

Self-reacting lymphocytes exist but are resistant to stimulation. Important for antigens only found in the periphery

117
Q

Immunological ignorance

A

Self-reactive cells present but do not mount a pathological response because the antigens are sequestered in immunologically privileged sites or require T cell help

118
Q

Suppression

A

Self-reactive B and T lymphocytes are present and potentially active but are kept in check by Treg cells

119
Q

Molecular mimicry

A

Past infection presented in a similar way to a self-peptide which causes cross-reactivity

120
Q

Natural autoantibodies

A

Some B cells in the healthy immune repertoire have the potential to produce autoantibodies
Usually IgM, low titre and low affinity
Thought to have a regulatory role or help dispose of breakdown products

Blood, Immunity and Infection (5 decks)

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