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Host Defense Exam 2 > Immune Complex Disease > Flashcards

Immune Complex Disease Flashcards

1
Q

What kind of hypersensitivity reaction is immune-complex mediated?

A

hypersensitivity type III

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2
Q

what are the pathological immune mechanisms in hypersensitivity type III?

A

immune complexes of circulating Ag and IgM or IgG

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3
Q

what is the mechanism of tissue injury and disease in hypersensitivity type III?

A

complement- and Fc receptor- mediated recruitment and activation of leukocytes

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4
Q

What are the types of hypersensitivity?

A

type I: immediate

Type II: antibody-mediated

Type III: immune complex-mediated

Type IV: T cell-mediated

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5
Q

What are the pathological immune mechanisms in immediate type I?

A

IgE antibody Th2 cells

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6
Q

What is the mechanism of tissue injury and disease in immediate type I?

A

Mast cells, eosinophils, and their mediators

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7
Q

What are the pathological immune mechanisms in antibody mediated type II?

A

IgM, IgG Ab against cell surface or ECM Ag

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8
Q

What is the mechanism of tissue injury and disease in antibody mediated type II?

A

opsonization and phagocytosis of cells

complement and Fc receptor mediated recruitment and activation of leukocytes

abnormalities in cell function

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9
Q

What are the pathological immune mechanisms in T cell mediated type IV?

A

CD4+ T cells (Th1 and Th17)

CD8+ CTLs

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10
Q

What is the mechanism of tissue injury and disease in T cell mediated type IV?

A

cytokine mediated inflammation

direct target cell killing, cytokine mediated inflammation

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11
Q

is type IV dependent on Ab?

A

no!

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12
Q

What is another name for type IV?

A

delayed hypersensitivity

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13
Q

What is a hypersensitivity reaction?

A

an exaggerated or misdirected immune response

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14
Q

What is an example of type I?

A

allergies/asthma

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15
Q

what is an example of type II?

A

immune thrombocytopenia

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16
Q

what is an example of type III?

A

lupus erythromatous

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17
Q

What is IC formation based on?

A

intensity of Ag sitmulus

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18
Q

What is the intensity of Ag stimulus based on?

A

type of Ag, length, route, and site of exposure to the Ag

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19
Q

What is the rate of IC formation dependent on?

A

the rate of Ab formation, Ab avidity, valence of Ag, and complement and Fc-FcR interactions

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20
Q

What influences the size and solubility of the immune complex?

A

complement and Fc-FcR interactions

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21
Q

what is the vigor of an immune response based on?

A

characteristics of antigen acting in concert with host factors, such as gender, age, MHC, etc.

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22
Q

What is valency?

A

how many identical epitopes are within an antigen

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23
Q

What are polyvalent Ags better at doing?

A

better immunogens and activators of immune functions

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24
Q

How do Ab affect IC formation?

A

via affinity and avidity

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25
Q

what is affinity?

A

how strong is the antibody binding site to a single epitope

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26
Q

what is avidity?

A

how strong is the overall attachment to the Ag

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27
Q

What is avidity affected by?

A

valency of the Ag and affinity of the Ab

28
Q

When do complexes form?

A

when soluble Ig bind polyvalent Ags they form complexes

29
Q

if there is Ab excess, what size complexes do you get?

A

small

30
Q

if there is Ag excess, what size complexes do you get?

A

small

31
Q

if there is Ag and Ab equivalence, what size complexes do you get?

A

large

32
Q

What leads to effector functions?

A

complexed Ab, not free Ab

33
Q

What is formation of IC based on?

A

specific binding between an Ag and and the Ag binding site

34
Q

What happens after, and only after, Ag binding?

A

biological activity mediated by Fc potion of complexed Ig molecule ensue

35
Q

What is the most important inflammatory reaction mediated by?

A

binding of Ag complexed with IgG to the Fc-gamma R on monocytes and neutrophils

36
Q

What else do ICs trigger?

A

complement

37
Q

What is the end result of IC formation?

A

generation of multiple inflammatory systems including interleukins, chemokines and the kinin and leukotriene cascades, which work in concert to mobilize neutrophils to the site of IC deposition, which is often times in small capillaries such as those found in the kidney or the joints.

38
Q

What kind of complexes are the most harmful?

A

the small complexes, as they can circulate, get trapped in vessels, & cause damage. The large complexes are easily removed by phagocytes

39
Q

When can small complexes cause a problem?

A

when antigenic stimulus doesn’t go away and excess small complexes can’t be cleared quickly enough

40
Q

What do Fc receptors on neutrophils and monocytes promote?

A

the uptake and catabolism of immune complexes

41
Q

how are immune complexes not catabolized on site transported, and where do they go?

A

transported via CR1 receptors on erythrocytes to the liver for disposal

42
Q

What does CR1 bind?

A

bound C3b

43
Q

What has CR1?

A

all erythrocytes, except platelets

44
Q

what does CR1 do to c3b during transport?

A

inactivates it –> converts it to iC3b

45
Q

What is an ITAM?

A

immunoreceptor tyrosine-based activation motif

BCR and it’s co-receptor: stimulated by Ag binding

innate cells and their activating FcR: stimulated by ICs

46
Q

What is an ITIM?

A

immunoreceptor tyrosine-based inhibition motif

found on B cells and other cells

can be stimulated by ICs via inhibitory FcR

47
Q

How do ITAMs mediate a B cell response?

A

Ag binds, cross links receptors, ITAMS phosphorylated on B cell receptor tails by Src family kinases, intracellular cascade, TF activated, inflammatory cytokines produced

48
Q

How does ITIM shut down a B cell response?

A

has Fc-gammaRIIB inhibitory Fc receptor, through which signaling will result in the dephosphorylation of proteins downstream

49
Q

What is the difference in affinity between Fc-gammaRI and Fc-gammaRIIB, and why is it important?

A

Fc-gammaRI has high affinity - low amounts of IC are sufficient to activate

Fc-gammaRIIB has low affinity - high amounts of IC needed for sustained activation

50
Q

What FcR’s are associated with ITAMS

A

1 and 3

51
Q

What FcR’s are associated with ITIMS?

A

2B

52
Q

What is an Arthus reaction?

A

a type III hypersensitivity reaction (immune complex mediated)

53
Q

How does an Arthus reaction occur?

A

local immune complexes and activation of complement releases inflammatory mediators c5a, c3a, and c4a, while c5a also induces mast cell degranulation. This results in inflammation, increased fluid and protein release, phagocytosis, and blood vessel occlusion

54
Q

What is systemic type III hypersensitivity?

A

complement and IC deposits cross linked to endothelial FcR and C3bR induces production of pro-inflammatory cytokines which recruits effector cells and releases damaging molecules which destroys tissue

55
Q

What does the time to, and severity of, clinical symptoms depend on in a systemic type III hypersensitivity?

A

depends on whether it is a primary (first exposure) or secondary response

56
Q

when can pathological inflammation, either local or systemic, occur?

A

when IC formation surpasses IC catabolism

57
Q

What are two possible causes of possible causes of IC production surpassing IC disposal?

A

intensity and duration of stimulus

impaired disposal: usually secondary to increased production of complexes and hepatic receptor saturation, CRI deficiency, medications. Also, small complexes are often not phagocytosed & tend to be deposited in vessels more than large complexes which are usually cleared.

58
Q

what do circulating ICs bind to, and where?

A

not efficiently trapped by the liver or spleen and bind to Fc-gammaR and C3b receptors at other sites, especially in the kidney/skin and synovium

59
Q

What is an arthus reaction?

A

a reaction that occurs when there are high levels of pre-existing antibodies to an antigen that is introduced at a site-usually under the skin. immediate, immense accumulation of immune complexes overwhelm the red cell transport system and there is rapid neutrophil activation as the complexes activate complement proteins and bind to neutrophil receptors. The activated neutrophils and other cells (most likely mast cells and basophils) release Il-8 and other vasoactive mediators that cause pain, swelling (increased fluid extravasation) and redness (increased blood flow) at the site of antigen injection.

60
Q

How do immune complexes activate cellular inflammation responses?

A

By crosslinking FcγR on multiple types of cells and stimulating the release of IL-8, a potent chemokine that recruits neutrophils to the area of FcR crosslinking.

61
Q

besides crosslinking FcgammaR, what else do immune complexes do?

A

classic complement pathway with subsequent generation of C3a, C567 and multiple other vasoactive molecules. Complement activation amplifies neutrophil recruitment to the area of immune complex deposition.

62
Q

If erythrocyte transfer to the liver cannot keep up with the formation of complexes at the site of formation, local accumulation of immune complexes leads to what?

A

neutrophil recruitment and activation

63
Q

When a IgG -IC targets an antigen to an Fcγ R on a macrophage, monocyte, neutrophil or dendritic cell, the cell is prompted to phagocytose the complex. What is this signal called?

A

ITAM

64
Q

When a IgG- IC targets an antigen to an Fcγ R on its B-cell, it activates what, and what does it do?

A

ITIM, which shuts down further B cell proliferation

65
Q

What cells are Fc-gammaRIIIB not on?

A

lymphoid

Host Defense Exam 2 (11 decks)

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