Term
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Definition
| Disease caused by antibodies, immune thrombocytopenia would be an example |
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Term
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Definition
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Term
| Hypersensitivity Type III |
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Definition
| Disease caused by antigen/antibody complexes, lupus erythematosus is a classical example |
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Term
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Definition
| Diseases associated with delayed hypersensitivity or TIMMI |
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Term
| What is IC formation dependent on? |
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Definition
| intensity of antigen stimulus: type of antigen, length of host exposure to it and the route and site of the exposure |
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Term
| What is the rate of IC formation dependent on? |
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Definition
- rate of antibody formation
- antibody avidity
- valence of antigen
- complement and Fc-Fc interactions that influence the final size and solubility of the immune complex. |
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Term
| What is the vigor of the immune response based on? |
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Definition
| = characteristics of the antigen acting in concert with host factors (gender, age, MHC and other immune loci) |
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Term
| What happens after FAB binding to antigen? |
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Definition
| - biologic activities mediated by the Fc portion of the complexed Ig molecule can begin. |
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Term
what is the most important inflammatory reaction mediated by?
What does this trigger? |
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Definition
binding of antigen complexed with IgG to FC-gamma receptor on monocytes and neutrophils.
- this binding triggers antimicrobial activites: phagocytosis, cytokine upregulation |
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Term
What does C3b bind?
What does this allow for? |
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Definition
CR1 on RBC for disposal in the liver
allows for very efficient removal of IC |
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Term
What do neutrophils do to reduce antigen exposure?
What else does this result in? |
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Definition
- destruction of antigen
- also decreases rate of IC formation |
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Term
| Steps for RBC binding and removal of IC's |
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Definition
1) small IC's form in the circulation and activate compliment
2) Many molecules of C3b are bound covalently to the IC
3) Bound Cb3 binds to teh CR1 on the erythrocyte surface, and C3b is converted to iC3b.
4) in the liver, phagocytic cells remove the immune complexes. |
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Term
| difference in dealing with IC's in liver and spleen |
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Definition
liver: destruction of IC's
Spleen: immune system mounts response to IC's but if it destroys them its to mount a B-cell response. |
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Term
| When do IC's cause a problem? |
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Definition
| if their rate of production is greater than their rate of destruction, pathological inflammation can occur, either locally or systemically. |
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Term
| Two main causes for production of IC exceeding disposal |
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Definition
1) intensity and duration of the antigenic stimulus leads to exuberant and prolonged production of specific antibody.
2 Impaired disposal caused by: hepatic receptor saturation, CR1 deficiency or mediactions |
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Term
| What is the cause of skin/synovial inflammation from IC's? |
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Definition
| Free IC's, not bound to RBC's, bind FC-gamma or C3b receptors at these sites because free IC's are not efficiently disposed of in the spleen or liver. |
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Term
| What does binding of IC's with FC-gamma receptors trigger? |
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Definition
| Release of IL-8 and recruitment of neutrophils |
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Term
What do free IC's activate?
What does this result in? |
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Definition
classical complement pathway
- results in increased C567 and other vasoactive molecules, further amplifying neutrophil recruitment to the area of immune complex deposition |
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Term
How is an arthus reaction different from a normal local immune complex inflammation reaction?
How can an arthus reaction occur clinically? |
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Definition
-arthus reaction requires pre-existing antibody to the antigen introduced at the site, while a normal local reaction does not.
- when a patient has been previously repeatedly immunized and is given the same vaccine again. |
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Term
| 4 Steps in arthus reaction |
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Definition
1) antibody to the antigen already present from past vaccinations
2) Vaccine antigen deposited by injection
3) Immediately overwhelmed CR1/RBC's
4) Massive neurtorphil activation and release of IL-8: pain, swelling, redness at site of antigen injeciton |
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Term
| How is an arthus reaction different from a systemic reaction? |
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Definition
| Arthus reaction occurs just at the site, whereas in a systemic reaction, IC's are throughout the circulation and deposition is typically in the skin, kidneys and synovium. |
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Term
| In theory, what effect will formation of IC's have on serum C3 and C4 concentrations? |
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Definition
| - they should decrease because complement is activated and these will be cleaved to C3a and C3b or C4a and C4b. |
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Term
| What follows the delivery of IC to the spleen or lymphoid tissue? |
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Definition
| IC's serve as stimulus for efficient antibody production |
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Term
| What is the role of activated complement components that are bound to IC's in the spleen? |
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Definition
| - serve as strong regulators of B-cell activation, differentiation and antibody formation. |
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Term
How is the result of IC-IgG binding to an APC Fcgamma Receptor different than the binding of IC-IgG to a B-cell?
What is the difference? |
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Definition
IC-IgG + APC FC-gamma receptor = activation of ITAM, facilitates antigen presentation.
IC-IgG + B-cell FC-gamma receptor = Activation of ITIM, shut down of further B-cell proliferation.
- In APC, affinity is very high and receptor can be activated with small amounts of IC.
- In B-cell affinity is very low and requires much greater amounts of IC. |
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Term
How is the B-cell ITIM-FCgammaR/IC-IgG useful clinically?
What is the result? |
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Definition
- Give anti Rh IgG to mother who is Rh- and pregnant with Rh+ child.
- Rh specific CD4 and memory B cells are not generated. |
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