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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
what is affinity?
how strong is the antibody binding site to a single epitope
26
what is avidity?
how strong is the overall attachment to the Ag
27
What is avidity affected by?
valency of the Ag and affinity of the Ab
28
When do complexes form?
when soluble Ig bind polyvalent Ags they form complexes
29
if there is Ab excess, what size complexes do you get?
small
30
if there is Ag excess, what size complexes do you get?
small
31
if there is Ag and Ab equivalence, what size complexes do you get?
large
32
What leads to effector functions?
complexed Ab, not free Ab
33
What is formation of IC based on?
specific binding between an Ag and and the Ag binding site
34
What happens after, and only after, Ag binding?
biological activity mediated by Fc potion of complexed Ig molecule ensue
35
What is the most important inflammatory reaction mediated by?
binding of Ag complexed with IgG to the Fc-gamma R on monocytes and neutrophils
36
What else do ICs trigger?
complement
37
What is the end result of IC formation?
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
What kind of complexes are the most harmful?
the small complexes, as they can circulate, get trapped in vessels, & cause damage. The large complexes are easily removed by phagocytes
39
When can small complexes cause a problem?
when antigenic stimulus doesn't go away and excess small complexes can't be cleared quickly enough
40
What do Fc receptors on neutrophils and monocytes promote?
the uptake and catabolism of immune complexes
41
how are immune complexes not catabolized on site transported, and where do they go?
transported via CR1 receptors on erythrocytes to the liver for disposal
42
What does CR1 bind?
bound C3b
43
What has CR1?
all erythrocytes, except platelets
44
what does CR1 do to c3b during transport?
inactivates it --> converts it to iC3b
45
What is an ITAM?
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
What is an ITIM?
immunoreceptor tyrosine-based inhibition motif found on B cells and other cells can be stimulated by ICs via inhibitory FcR
47
How do ITAMs mediate a B cell response?
Ag binds, cross links receptors, ITAMS phosphorylated on B cell receptor tails by Src family kinases, intracellular cascade, TF activated, inflammatory cytokines produced
48
How does ITIM shut down a B cell response?
has Fc-gammaRIIB inhibitory Fc receptor, through which signaling will result in the dephosphorylation of proteins downstream
49
What is the difference in affinity between Fc-gammaRI and Fc-gammaRIIB, and why is it important?
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
What FcR's are associated with ITAMS
1 and 3
51
What FcR's are associated with ITIMS?
2B
52
What is an Arthus reaction?
a type III hypersensitivity reaction (immune complex mediated)
53
How does an Arthus reaction occur?
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
What is systemic type III hypersensitivity?
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
What does the time to, and severity of, clinical symptoms depend on in a systemic type III hypersensitivity?
depends on whether it is a primary (first exposure) or secondary response
56
when can pathological inflammation, either local or systemic, occur?
when IC formation surpasses IC catabolism
57
What are two possible causes of possible causes of IC production surpassing IC disposal?
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
what do circulating ICs bind to, and where?
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
What is an arthus reaction?
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
How do immune complexes activate cellular inflammation responses?
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
besides crosslinking FcgammaR, what else do immune complexes do?
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
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?
neutrophil recruitment and activation
63
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?
ITAM
64
When a IgG- IC targets an antigen to an Fcγ R on its B-cell, it activates what, and what does it do?
ITIM, which shuts down further B cell proliferation
65
What cells are Fc-gammaRIIIB not on?
lymphoid

Host Defense Exam 2 (11 decks)

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