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General Med 1 > Path - Anatomy, Inflam and Immu - Exam 2 > Flashcards

Path - Anatomy, Inflam and Immu - Exam 2 Flashcards

1
Q

Describe possible outcomes for a cell subjected to stress - there are 3

A
  1. Adaption and improved funtion
  2. Reduced health followed by recovery to the same level
  3. With persistent stress, cell injury and/or death
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2
Q

Give an example of a physical, environmental, genetic and immune function stimuli that may cause cellular injury

A

Physical - mechanical/heat
Env. - bacterial
Genetic - inherited
Immune function - auto-immune

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3
Q

What is the connection between pathogenesis and morphology?

A

Pathogenesis causes changes in morphology

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4
Q

Describe features commonly found in injured cells - reversible

A

Swelling, cytoplasmic inclusions, accumulations and pigments, steatosis

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5
Q

Describe features commonly found in injured cells - irreversible

A

Abnormal mitochondria, irregular cell contours, eosinophilia and nuclear deformities

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6
Q

How can swelling of the cell occur, and what does it look like?

A

Can occur through failure of a membrane pump, or could be adaptive - this is called membrane blebbing and can occur in hypoxia to increase surface area, facilitating uptake of oxygen.

Swelling in toxic injury: cell looses organised structure, ribosomes detach and lipid accumulates.

Hydropic swelling makes a cell look pale and washed out
Excess liquid in cell dilates the cell substructure. ER is completely disrupted

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7
Q

What are inclusions?

A

Something that’s not usually present, and is described according to staining properties e.g. a Hyaline inclusion would be glassy and pink in appearance.
An example of an inclusion is a Mallory body, often found in alcoholic livers.
However, they can also be viral

  • eosinophilic, basophilic or amphiphilic
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8
Q

What are accumulations?

A

A build up of a product of the body, which should not be there.
These can be intracellular or extracellular.
Intracellular: glycogen accumulates in the lysosome in alpha-gluconidase deficiency

Extracellular: amyloid can get deposited in the myocardium, which will eventually interfere with vascular supply

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9
Q

What are pigments?

A

Coloured substances, which can be endogenous or exogenous
Endogenous - normally present, abnormally accumulated
Exogenous: not normally present

endogenous = normally present but abnormally accumulated. Haemachromatosis - too much haemosiderin (stored iron) in liver cells

Exogenous”
- ferruginous bodies (asbestos fibbers coated in iron)

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10
Q

Describe Steatosis, and where it is particularly relevant

A

Steatosis - steahepatitis - cirrhosis - liver failure

Steatosis is the abnormal accumulation of lipid.
Organs may appear enlarged and yellow in appearance, with abnormally large lipid droplets displaying mitochondria clustered around them.
Benign in isolation, but it does sensitize cells to inflammation, which can lead to hepatitis, then cirrhosis, then fatal liver failure

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11
Q

Why might mitochondria appearance change, and what could this change look like?

A

Mitochondria can change in response to Anoxia - absence of oxygen
They become greatly swollen and lose their parallel arrays of cistaes

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12
Q

Why would Eosinophilia be seen in irreversible cell injury?

A

Denatured proteins in the cytoplasm of cells bind eosin, and less RNA production leads to loss of basophilia

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13
Q

What is a nuclear abnormality we might see in irreversible cell injury?

A

Multinucleation - nuclei divide without cell pulling them apart

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14
Q

What could happen to cell membranes and cell staining in irreversible cell injury?

A
  • Irregular contours

- Eosinophillia as a result of released protein into the cell

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15
Q

Define necrosis

A

The spectrum of morphological changes following cell death or tissue death. Always a pathological process

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16
Q

When do you see microscopic changes in cells undergoing necrosis, and what is the sequence of nuclear changes you will see?

A

-4-12 hours

  • Nucleus will go from normal, to Pyknosis as a result of shrinkage, darkening and condensation (black dot). From there, to Karyorrhexis, which is breakdown of the nucleus. This is followed by Karyolysis, where the nucleus is gone
  • Throughout this process, the cell will become more and more eosinophilic
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17
Q

What are some other microscopic changes you will see in necrotic tissue?

A

Cytoplasmic vacuolation
Eosinophilia
Cell membrane blebbing/rupture

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18
Q

Describe coagulative necrosis

A
  • Most common type
  • Usually follows ischaemia, which causes an infarct (localised necrotic area). Tissue is softer than normal, and either more pale (pale infarct) or haemorrhagic (red). Over time, a haemorrhagic border will develop around a pale infarct.
  • The cellular architecture is preserved, and cell outline remains for days/weeks. –There is a delayed breakdown of cells, and an inflammatory response.
  • Histologically you might see pink cytoplasms still in the shape of cells, missing nuclei.
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19
Q

Describe colliquative necrosis

A
  • The necrotic cell releases powerful hydrolytic enzymes, as well as inflammatory exudate - particularly neutrophils. This leads to liquefaction of the entire cells. Later on, there is an inflammatory reaction and liquid material is removed by macrophages, leaving a cystic space, often with a fibrous peripheral border.
  • Cellular architecture almost completely disintegrates
  • Occurs in two main settings: the brain, or an abscess cavity in the lung
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20
Q

Describe Caseous necrosis

A

-Almost exclusively in TB patients
-Has a white, cheesy appearance
Microscopically is an amorphous, granular debris, lacking in cell detail and outline. H&E sections will show eosinophilia.
-Usually have granulomatous adjacent inflammatory reactions i.e. giant cells and macrophages everywhere
-Histological sections will show the absence of cell outlines and tissue destruction

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21
Q

What is the difference between wet, gas and dry gangrene?

A
  • Wet gangrene is necrosis with superadded putrefaction, usually due to gram negative bacteria
  • Gas gangrene is usually due to gram-positive bacteria found in soil, like Clostridium species. It causes crepitant swelling
  • Dry gangrene is essentially mummification - tissue is dry and black. Often a result of coagulative necrosis
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22
Q

What does fat necrosis look like from a macroscopic perspective?

A

Chalky deposits, as a result of released fatty acids reacting with calcium

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23
Q

What are the outcomes of necrosis dependent on?

A

The tissue involved: susceptibility to injurious stimuli and ability to regenerate, extent of necrosis, and time elapsed.
Subsequent fibrosis is often seen

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24
Q

What is autolysis?

A

Self-digestion of tissue AFTER DEATH, not technically necrosis

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25
Q

What is the difference between innate and adaptive immunity?

A

Innate immunity is immediate in response to infection, using relatively non-specific defence mechanisms. It activates and orientates the adaptive immune response.
Adaptive immunity ‘tailors treatment’

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26
Q

What is the innate immune response made up by?

A
  • Physical barriers including skin and saliva
  • Soluble proteins in the tissues and circulation e.g. complement and acute phase proteins
  • Cellular components including neutrophils and macrophages
  • Cytokines released by cells - IFN-gamma and TNf-alpha
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27
Q

How does the innate system recognise non-self?

A

Through pattern recognition receptors, which recognise altered cells, oxidised cells, oxidised membrane structures etc
In infections, patterns recognised are those conserved in non-human cells e.g. Pathogen associated molecular patterns (PAMPs)

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28
Q

What to Toll-like receptors (TLRs) do?

A

These are located on the cell surface and in walls of intracellular vesicles, particularly in macrophages and dendritic cells. They recognise a range of pathogen-associated molecules from bacteria and viruses
They activate other molecule to induce the production of PRO-inflammatory cytokines and chemotactic factors

  • recognise PAMPs
  • activate TF to induce pro-inflam cytokines and chemokines and IFN
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29
Q

What do NOD-like receptors do?

A

Act as intracellular sensors of bacterial infection. They’re located in the cytoplasm of cells routinely exposed to bacteria e.g. epithelial cells of the gut, dendritic cells and macrophages

Crohns = loss of function of NOD2

NALP3 - senses cellular damage (DAMPs)

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30
Q

What are some of the consequences of production of Pro-inflammatory cytokines (e.g. IL-1B/IL-6/TNF-a)?

A

Activation of complement opsonization, phagocytosis, decreased bacterial and viral replication and initiation of adaptive immune response

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31
Q

What do levels of C-reactive protein tell you?

A

This is a pro-inflammatory acute phase protein, and an important opsonin, so levels of it rise with an infection
High levels of CRP therefore tell you the body is fighting inflammation

  • best marker
  • produced by liver under influence of IL 6

EXCEPTIONS:

  • SLE
  • sjorgens
  • UC
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32
Q

What happens to Neutrophils during inflammation/infection?

A

Neutrophils normally roll along a vessel’s endothelium. During inflammation, stronger adhesion molecules are expressed on endothelium, anchoring neutrophils to vessel wall. They then extravasate, squeezing between endothelial cells and traverse the basement membrane. They then ride a chemokine gradient to the site of inflammation

  • P and E selectin - Sialyl Lewis - weak adhesion
  • ICAM 1 - LFA-1 - extravasation
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33
Q

What’s the process of phagocytosis?

A
  • Phagocyte receptors bind to microbial surface components
  • Bound pathogen is internalised into a phagosome
  • Pathogen is killed either by phagosome acidification or through fusion with lysosome
  • Soluble debris undergoes exocytosis
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34
Q

What are the three major classes of innate phagocytes?

A
  1. Granulocytes: neutrophils, basophils and eosinophils. Neutrophils are recruited early and die early
  2. Macrophages
  3. Immature dendritic cells
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35
Q

What are the main cells involved in adaptive immunity?

A

T cells
B cells
Plasma cells

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36
Q

When does adaptive immunity kick in?

A

After about 12 hours, at which stage it is properly primed.

It proliferates within 1-3 days, and the makes antibodies which recognise the extracellular pathogen.

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37
Q

How are T-helper subsets divided?

A

Based on the transcription factor they carry, which dictates their function

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38
Q

What are the different subsets of THs?

A
  1. TH1
    - caused by IL-12
    - intracellular pathogens: parasites and bacteria
    - autoimmunity
    - delayed type hypersensitivity
  2. TH2:
    - caused by IL-4
    - extracellular pathogens: viruses and bacteria
    - allergy, asthma
  3. TH17
    - caused by TGF-B
    - extracellular pathogens: fungi and bacteria
    - autommunity
  4. TFH - follicular
  5. Treg (FOXP3)
    - caused by TGF-B
    - immunosupression
    - developed in thymus due to self tolerance
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39
Q

PAMP examples:

A

Flagellin

dsRNA

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40
Q

What does co-stimulation do to T-cells?

A

Acts as a mechanism to avoid auto-immunity

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41
Q

What does Tolerance do with T-cells?

A

Prevents auto-immunity

Central tolerance takes place in generative lymphoid organs - bone marrow and thymus.
Outcomes:
a) apoptosis
b) change in receptors
c) development of regulatory T cells = CD4+

Peripheral:

a) anergy
b) apoptosis
c) supression

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42
Q

What are the lymphoid organs?

A

Primary and secondary

  1. Primary - development and maturation.
    Thymus and BM
  2. Secondary - trap antigens
    Lymph, spleen, tonsils, gut etc
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43
Q

What does the thymus do in central tolerance?

A

Displays peripheral tissue antigens in thymic medullary epithelial cells

AIRE = transcriptional regulation

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44
Q

What is the connection between B cells and antibodies?

A

Antibodies are only produced by B cells that respond specifically to one antigen

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45
Q

What are some of the effector functions of antibodies?

A
  • Neutralisation of microbes
  • Opsonization and phagocytosis of microbes
  • Complement cascade activation
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46
Q

what is innate immunity

A

always present (ready to attack); many pathogenic microbes have evolved to resist innate immunity

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47
Q

what is adaptive immunity

A

stimulated by exposure to microbe, more potent

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48
Q

what are lymphocytes

A

cells of the adaptive immunity, recognise antigens and develop into cells that perform defence functions

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49
Q

what re antigen presenting cells

A

cells that capture antigens and display them to lymphocytes, interphase between innate and adaptive immunity

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50
Q

what are effector cells

A

leukocytes (white blood cells) that eliminate microbes, may be lymphocytes but are often leuockotes (e.g. phagocytes, innate immune cells)

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51
Q

how are lymphoid organs classified

A

2 groups, primary and secondary

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52
Q

what is the primary lymphoid organs roles

A

provides an appropriate microenvironment for the development and maturation of lymphocytes, bone marrow and thymus

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53
Q

what is the secondary lymphoid rogans role

A

traps antigens, generally from nearby tissues/fluid and are sites where lymphocytes can effectively interact with antigens (lymph node, spleen etc.)

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54
Q

helper T lymphocytes can produce ______ to have what effects

A

cytokines to activation macrophages, inflammation edna citation of T and B lymphocytes

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55
Q

what is the role of the B lymphocytes

A

secretion of antibodies and this causes neutralisation of microbes, complement activation and pahgocytosis

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56
Q

what is the role of the cytotoxic T lymphocyte and the natural killer cell

A

killing of the infected cell

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57
Q

What are needed to initiate immune responses and how

A

APC, co-localize with T cells and display HLA molecules that interact with T cell receptors (class 1 and class 2)

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58
Q

conseuqnce of mutations in AIRE

A

human disease, autoimmune polyendocrinopathy with candidiasis and ectodermal dysplasia, also called autoimmune polyendocrine syndrome.

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59
Q

naive T cells can be primed by what

A

dendritic cells

60
Q

what are the functions of antigen-presenting cells

A

capture antigens and take them to correct place, display antigens in a form that can be recognised by specific lymphocytes (T cells are MHC- associated peptides and B cells are native antigens), Provide secondary signals for T cell activation

61
Q

Where are dendritic cells found

A

at sites of microbe entry

62
Q

what are the receptors on dendritic cells

A

TLR and tohers

63
Q

what are the 4 subsets of dendritic cells

A

classical (role in presentation), plasmacytoid (source of type 1 IFN), immature (in tissues, role in presentation of self antigen and maintain of tolerance ), mature (activated by TLR and other signals, role in T cell activation)

64
Q

what could be the four outcomes from B cell activation and antibody production

A

a) antibody secretion
b) isotope switching
c) affinity maturation
d) memory B cell

65
Q

what are the two B cell subsets

A

T dependent (isotope switched, high affinity antibodies, long lived plasma cells, follicular B cells) T independent (mainly IgM, short-lived plasma cells, marginal zone B cells and B1 B cells)

66
Q

What are the two MHC classes?

A
  1. MHC Class I
    - antigen in cytosol
    - cytotoxic T cells
  2. MHC Class II
    - antigen in vesicle
    - TH
67
Q

What are five components of innate immunity?

A

Epithelial barriers, dendritic cells, phagocytes, complement cascade and NK cells

68
Q

How many days after infection do we see antibodies from B cells and Effector T cells?

A

About 5

69
Q

What do macrophages and dendritic cells do?

A

They are phagocytic cell and professional antigen presenting cells. They recognise MAMPS via PRRs (pattern recognition receptors)

70
Q

What role do epithelial cells play in the innate immune system?

A

They are sentinel cells, recognising PAMPS and responding with inflammatory mediators

71
Q

What do natural killer cells do?

A

Kill damaged or virus infected cells, in an action similar to cytotoxic T cells

72
Q

What happens when P/MAMPS are recognised by PRRs?

A

PRRs induce endocytic activation and signal transduction, turning on immune mediator production and/or phagocytosis. This causes antigen capture, phagocytosis, opsonization, antigen presentation, complement activation, kinin production, cytokine response, removal of pathogens cytolytic killing of pathogens and activates adaptive immunity

73
Q

What are the six main cells of the adaptive immune system?

A

Antigen-presenting cells: capture, digest and present epitopes to T cells, activating adaptive immunity
B cells - produce and secrete antibodies
Plasma cells - Activated B cells, producing antibodies
T-Helper cells - Help B cells produce antibodies, help macrophages kill bacteria, and promote or suppress other immune functions
T-regulatory cells - Active suppression of immune responses, tolerance
Cytotoxic T-cells - detect and kill infected cells

74
Q

Which cells recognise a pathogen in the adaptive immune system?

A

TCRs (T cell receptor) and BCRs. Each B and T cell will express a unique receptor

75
Q

What are the differences in speed of response in innate vs adaptive immune system?

A

Innate: quick acting all the time, broad specificity
Adaptive: relatively slow on first exposure to antigen, quick for following exposures. Highly specific

76
Q

What are the four professional antigen presenting cells, and why are they called professional?

A 
Monocytes, macrophages, B cells and dendritic cells
Professional because they present the antigen to the TCR via the MCH class II molecule Other cells don't use class II, they use class I.
77
Q

What is humoral immunity mediated by?

A

Macromolecules. It is found in extracellular fluids i.e. secreted antibodies, complement proteins and certain antimicrobial peptides

78
Q

Macromolecules. It is found in extracellular fluids i.e. secreted antibodies, complement proteins and certain antimicrobial peptides

A

Activation is initiated by specific recognition of antigens on the surface Ig receptors of the B cells. The recognition of the antigen, along with T-helper cells, stimulates the proliferation and differentiated of the specific B cell clone. Progeny of the clone may produce antibodies, undergo affinity maturation, or persist as memory cells

79
Q

What are the five T-helper subsets?

A

Th1 - protects against intracellular pathogens
Th2 - protects against extracellular pathogens
Th17 - protects against extracellular pathogens
Treg - Immunosuppression
T follicular helper cells - trigger and maintain germinal centres

80
Q

Describe the process by which dendritic cells prime Naive T cells

A
  1. Antigen capture by DC
  2. Loss of DC adhesiveness and migration of DC
  3. Maturation of migrating DC as it passes through afferent lymph vessel. Degrades antigen and presents as epitope
  4. Mature dendritic cells presents antigen to naive T-cell
81
Q

What are the acute phase proteins?

A

CRP, manose-binding lectin and fibrinogen

82
Q

Define: pleiotropism, redundancy, synergy, antagonism

A

Pleiotropism -> activate numerous types of responses - differentiation, growth, activation and chemotaxis
Redundancy -> functional overlap
Synergy -> between cytokines to optimise response
Antagonism -> to regulate duration and potency of response in order to prevent autoimmunity

83
Q

What are cytokines?

A

Secreted proteins that mediate and regulate immunity (innate and adaptive immunity) and inflammation

84
Q

Cytokines can act in an autocrine, paracrine and endocrine manner. What are these?

A

Autocrine - acts on cell that synthesized them
Paracrine - cells in the immediate environment
Endocrine - distant cells - similar to hormone

85
Q

What are the 3 types of interferon?

A

IFN alpha/beta/gamma

86
Q

What is the purpose of colony stimulating factor (CSF)?

A

Differentiates bone marrow cells to particular cells but can also have effects on mature cells

87
Q

What are the different cytokine families?

A
  • IL
  • IFN
  • TNF
  • CSF )colony stimulating factor) - differentiated B cells
    Growth factors, i.e. TGF
88
Q

What are chemokines?

A

Small proteins with 2 internal disulfide brides and conserved structure that act as chemoattractants when bound to a specific receptor - help cells move to SPECIFIC places

89
Q

Is the direction of chemotaxis towards higher or lower chemokine concentration?

A

Higher

90
Q

What are the 4 families of chemokines and what differentiates them?

A

C, CC, CXC, CXXXC - categorised based on spacing of the 2 cysteines

91
Q

What are complement proteins?

A

Heat labile plasma proteins activated in under certain situations that act as effector mechanisms for the innate immune system and humoral adaptive immune system

92
Q

What 5 functions do complements perform in innate host defence?

A

Innate: Opsonisation, Initiate inflammatory response, Clearance of apoptotic debris

Adaptive: B-cell activation, T-cell priming

93
Q

What are the 3 major pathways of the complement system?

A

Classical (antibodies), Alternative (bind to microbe), Lectin (bind to mannose)

94
Q

Which is the MAIN complement protein common to all pathways that INITIATES late steps of the process?

A

C3b

95
Q

In a clinical complement assessment, which two complement proteins are measured?

A

C3 and C4 serum levels

96
Q

Are high C3 levels pathogenic?

A

No, mostly part of the acute phase response

97
Q

What is the most likely infection to result from lack of C5-9 function?

A

Neisserial bacterial infection

98
Q

Do antigen presenting cell produce cytokines?

A

Yes aka dendritic cells, B cells, macrophages all produce cytokines

99
Q

What are some of the roles cytokines help with?

A
  • Antigen recognition in lymphoid organs
  • T-cell expansion and differentiation: each step of the T-lymphocyte life cycle is regulated by a cytokine
  • Supporting effector phase of T-cell response
100
Q

What are corticosteroids?

A

alter gene transcription - suppression of pro-inflammatory genes

101
Q

What is humoral immune responses to infections as a broad definition?

A

Innate and adaptive immune responses mediated by soluble (cell-free) immune system

102
Q

Fill in the blank:

Bacteria induce ____ to produce ____, which acts on ____ to induce synthesis of ____-____ proteins.

A

Bacteria induce macrophages to produce IL-6, which acts on hepatocytes to induce synthesis of acute-phase proteins.

103
Q

Does C-reactive protein bind to phosphocholine on bacterial surfaces? If yes, what does CRP act as?

A

Yes, it acts as an opsonin and complement activator.

104
Q

MBL (mannose-binding lectin) binds to carbohydrates on bacterial surfaces. True or false?

A

True

105
Q

What are the 4 ways in which a microbe can evade complement activity?

A
  1. Inhibit alternative pathway of complement activation
  2. Inactivate complement components
  3. Bind plasma proteins that negatively regulate complement activity
  4. Impair opsonisation and phagocytosis
106
Q

What is the structure of an immunoglobulin?

A

It has an antigen binding domain, a complement binding site and placental transfer site - the last 2 binds to Fc receptors

107
Q

What is the relationship between hemagglutination-inhibiting antibodies and protection against influenza?

A

Higher hemagglutination-inhibiting antibodies numbers in the body increases the level of protection against influenza.

  1. HA1 glycoprotein - blocks binding to sialic acid on host cell membrane
  2. HA2 - inhibits fusion to endosomes
  3. neuraminidase - prevents release of new viruses from infected cells
108
Q

How does opsonisation enhance phagocytosis?

A

The microbe is coated with opsonising antibodies. This can bind to opsonin receptors on the phagocyte, with co-stimulation of PRRs (pattern recognition receptors) of the phagocyte by the microbe leads to enhancement of lysosomal degradation of the microbe.

109
Q

Are elderly adults with lower opsonophagocytic antibody more susceptible to pneumococcal disease?

A

Yes - low opsonophagocytic antibodies are strongly correlated with low IgG antibody activity

110
Q

What are four mechanisms by which the complement pathway controls infection?

A
  1. Activates MAC to lyse bacteria
  2. Opsonizes pathogens
  3. Actives inflammatory response by triggering release of histamine from mast cells
  4. Enhances clearance of antigen-antibody complexes
111
Q

What are some of the roles of antibodies in an immune response to a pathogenic microbe?

A 
Neutralize bacterial toxins and viruses
Opsonize particles
Activate complement
Activate NK cells
Activate basophils and eosinophils
112
Q

Which receptors on a phagocyte recognises an opsonized cells?

A

C3b & Fc-epsilon

113
Q

What happens to a mast cell on recognition of a pathogen?

A
  1. Triggers innate receptors and degranulation of the mast cells
  2. Mast cell goes to adaptive IS, and T/B/plasma cells sensitize the mast cells with pathogen specific IgG or IgE. There is then proliferation of these mast cells
114
Q

What are some effects of Mast cell activation?

A

Contraction of smooth muscle, recruitment of dendritic cells, activation of macophages

115
Q

Which cells initially respond to a Candida albicans infection?

A

CD4, neutrophils, macrophages, monocytes and DC

116
Q

Which interleukin causes Th17 production?

A

IL-6, which leads to neutrophil activation

117
Q

Which interleukin causes Th2 production?

A

IL-4

118
Q

How does a T-cell and natural killer cell recognise a virally infected human cell?

A

Normal human cells express human leukocyte antigens (HLA) on their surface, which T-cells recognise.
Virally infected cells have downregulated HLA, and express viral peptides on the surface.
T-cells recognise the foriegn material, and NK cells recognise the HLA downregulation

119
Q

Which APC educates CD8+ cells, and which MHC class are CD8 cells?

A 
Dendritic cells
CD8+ cells are MCH class 1
120
Q

What type of antibody neutralises rotaviruses?

A

Mucosal IgA

121
Q

What are the functional effects of the hum moral immune system?

A
  1. neutralisation of bacterial toxins and viruses
    - IgA
    - i.e. Flu, HIV, Rotavirus
  2. Opsonisation
    - IgM and IgG2
  3. Activation of complement cascade
  4. Activation of NKCs
  5. Activation of basophils/mast cells
  6. Activation of eosinophil
    - IgE
    - parasites and Helminths
122
Q

What causes malaria?

A
  • plasmodium falciparum
  • bite deposits sporozoites in blood sream - liver
  • hepatocytes rupture and release merozoites into blood
  • second bite
  • some merozoites develop into gametocytes in RBCs, therefore complement activation to protect RBCs.
  • in prince of complement, antibodies can interact with complement factors to prevent invasion of RBC directly and lyse merozoite
123
Q

What causes schistosoma Mandonii?

A

Snail one

  • parasite nematode - allergens - DC or macropgase which present it to native t cell - effector t cell
  • IL4 and IL5 (and IgE) - eosinophil degranulation and parasite killing
124
Q

Where does a baby get its Ig from?

A

Pregnancy:
IgG from placenta

After birth:
IgA from breast milk

125
Q

What are the different Igs?

A

IgD - B cell receptor
IgA - mucosal antibodies
IgM - Bcell receptor, agglutination and opsonisation
IgG - complement, cell activation, opsonophagosite
IgE - mast cells/eosinophils

126
Q

What are the effects of mast cells releasing IL-6?

A
  • Il-6 - hepatocytes synthesise acute phase proteins.

CRP and MBL - opsonin and complement activator. Both bind to bacterial surface

127
Q

What are 4 cellular immune responses to pathogens?

A
  1. Lysis of infected cells by cytolytic lymphocytes
  2. Activation of monocytes and macrophages
  3. Activation of neutrophils and eosinophils
  4. Granuloma formation to contain the infection
128
Q

What is the innate and adaptive mechanisms for the cellular response: Lysis of infected cells by cytolytic lymphocytes?

A

Innate: Natural Killer Cells

Adaptive: CD8+ T-cells

129
Q

What is the innate and adaptive mechanisms for the cellular response: Activation of monocytes and macrophages?

A

Innate: Directly via PRRs

Adaptive: IFNgamma from CD4+ T-cells

130
Q

What is the innate and adaptive mechanisms for the cellular response: Activation of neutrophils and eosinophils?

A

Innate: Directly via PRRs

Adaptive: IL-17 and IL-22 from CD4+ T-cells

131
Q

What is the innate and adaptive mechanisms for the cellular response: Granuloma formation to contain the infection

A

Innate: N/A

Adaptive: IFNgamma from CD4+ T-cells

132
Q

What types of invasive candida infections can you get?

A 
•  Acute mucocutaneous infecDon
•  Chronic mucocutaneous candidiasis
•  Systemic candidiasis 
– Skin
– Eye
– Liver and spleen 
– Kidney
133
Q

What are the immune evasion strategies of Candida albicans?

A
  • Inhibition of complement activation and complement receptor function
  • inhibition of phagocytosis by macrophages
  • inhibition of intracellular killing mechanisms in macrophages
  • inhibition of pro-inflammatory cytokines AND secretion of anti-inflammatory cytokines
134
Q

What causes the antigenic variation of HIV that allows it to evade the immune system?

A
  • high mutation rate

- lots of recombination

135
Q

How does a tuberculin skin test work?

A

It tests the CD4 T-cell response. It is a delayed type hypersensitivity response to tuberculin. If you have CD4 cells that recognise the bacteria then you will get an active response.

136
Q

How does Mycobacterium tuberculosis evade macrophages?

A

How does Mycobacterium tuberculosis evade macrophages?

137
Q

What are the disease causing immune responses?

A

Type I: Immediate Hypersensitivity reaction (allergy/atopy)
- IgE

Type II: antibody mediated disease

  • IgG or IgM
  • host cell

Type III: immune complex mediated disease

  • IgG
  • complex deposits in vessels, mainly kidneys and synovium (joints) - inflammation

Type IV: T cel mediated (delayed type)
- Memory TH1

138
Q

What are the characteristics of type I?

A
  • rapid
  • directed against antigens
  • involves masts, IgE and antigen

a) sensitisation and memory:
DC - MHC II - Naive T cell - TH2. OR IgE memory B primes TH2.
TH2 releases IL-4 and IL-13 which results in:
i. IgM naive B - IgE memory (isotype switching)
ii. IgE memory B cell

b) immediate phase:
- masts and bs bind IgE via Fc(E) receptors
- antigen causes cross linking of IgE
- masts and bs degranulate

c) late allergic inflammation mediated by TH2
- 6hr - ns and bs
- 24 hrs - es
>24 hrs - lymphocytes
- can lead to chronic inflammation and tissue remodelling

139
Q

What are the characteristics of type II?

A
  • antibody mediated
  • own cells OR blood transfusions

a) autoimmune haemolysis:
i. IgM - agglutinates RBCs and complement - rapid destruction
ii. IgG - Fc receptors in splenic macros bind to IgG coated RBC - gradual destruction

b) allo-immune haemolysis:
ABO mismatch

c) Rh
- ve woman carrying 2nd+ +ve baby
- treat with anti-Rh IgG

d) myesthenia gravis
- autoantibodies against AChR in postsynaptic cleft of neuromuscular junction

140
Q

What are the characteristics of type III?

A
  • immune complex mediated

USUALLY:

  • broken down due to C3b
  • RBCs express CR1 for activated C3b, therefore complexes coated by C3b bind to CR1
  • phagocytosed in liver and spleen macrophages
BUT FAILURE:
- deposition in BVs, especially kidneys and synovium.
Therefore:
- vasculitis
- arthritis
- nephritis
  • PMNs and monocytes
141
Q

What are the characteristics of type IV

A
  • T cell mediated (delayed)
  • T cell sensitised to antigen
  • secondary exposure - releases lymphokines - macros - inflammation

a) auto
b) hypersensitivity

I.e. TB - granulomatous inflammation

  • CD4+ and CD8+ release cytokines which result in inflammation
  • AND CD8+ kill cells directly
142
Q

Why are most transplants rejected?

A
  • adaptive immune system

- MHC is the principal antigenic barrier

143
Q

What is the difference between direct and indirect rejection?

A

a) direct:
T cell recognises aloo-MHC

b) indirect:
Dendritic cells present it

144
Q

What are the types of rejection reaction?

A
  1. Hyperaccute - minutes
    - preformed antibodies (i.e. previous transfusion)
    - thrombosis of graft vessels
    - ischaemic necrosis
  2. Acute - days-weeks
    - CD4 cytokines and CD8 destruction
  3. Chronic - months-years
    - progressive loss of function
145
Q

What are four effects of cytokines?

A
  • chemotaxis
  • cell activation
  • differentiation
  • growth
  • acute-phase proteins in liver
  • increased body temp (hypothalamus)

General Med 1 (24 decks)

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