Term
| What are the functions of immunoglobulins? |
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Definition
1) opsonize bacteria
2) neutralize toxins
3) activate complement
4) activate mast cells
5) activate NK cells |
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Term
| What are hypersensitivity reactions via IgE? |
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Definition
| IgE activates mast cells, potentially leading to allergic rhinitis, asthma, or systemic anaphylaxis |
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Term
| How does IgG interact with cell- or matrix-associated antigens? |
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Definition
| It binds them to activate complement and Fcy-R+ cells like phagocytes and NK cells, alters signaling, and is related to drug allergies |
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Term
| What is a cause of serum sickness? |
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Definition
| IgG-antigen immune complexes can deposit and cause complement and phagocyte migration to the area |
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Term
| What activates macrophages? Eosinophils? |
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Definition
| TH1-cells activate macrophages; TH2-cells activate eosinophils |
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Term
| What is the role of Fcy receptors? |
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Definition
| Directing phagocytic cells and NK cells to specific pathogens to facilitate opsonization |
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Term
| How do NK cells identify their target? |
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Definition
| Through antibody-dependent cellular cytotoxicity (ADCC) or lost expression of MHC molecules |
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Term
| What do macrophages and neutrophils use to bind complement? |
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Definition
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Term
| Which Ig is a first line barrier and why? |
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Definition
| IgA; it is responsible for mucosal antibody mediated immunity and is present in the mucous surfaces lining entryways to the body |
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Term
| What mediates class switch to IgA in B cells? |
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Definition
| TGF-B and IL-5 from CD4 TH2-cells |
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Term
| What shape does IgA take? |
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Definition
| It forms a dimer using a J-chain |
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Term
| How does IgA remain localized and protected from proteolysis? |
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Definition
| It passes through basement membranes and binds to a poly-Ig receptor for endocytosis. With the receptor, it is transported in protective vesicles to the lumen, where the receptor is cleaved leaving a secretory component attached to free IgA |
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Term
| What carries IgG from the lumen across the endothelium and into extracellular spaces? |
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Definition
| FcR-Brambell (FcR-B). This is also how IgG crosses the placenta |
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|
Term
| What mediates class switch to IgE in B cells? |
|
Definition
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Term
| How do mast cells and basophils attach to monomeric IgE molecules? |
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Definition
| They have FcE receptors with high affinity for monomeric Fc regions of IgE molecules. This makes them "pre-armed" with IgE even when antigens are not present |
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Term
| What causes granule content release? |
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Definition
| Multivalent antigen-binding that results in cross-linked IgE |
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Term
| What granules are released and what is the effect? |
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Definition
| Histamine, heparin, and TNF-a cause an immediate hypersensitivity reaction of vascular permeability, smooth muscle contraction, and inflammation |
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Term
| What do leukotrienes (LTKs) do? |
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Definition
| They cause smooth muscle contraction and increased vascular permeability; they are synthesized late along with IL-4 after mast cell activation |
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Term
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Definition
| C3a, C4a, and C5a, which can also cause mast cell degranulation by activating mast cells |
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Term
| How are pathogens expelled from the GI tract? From the airways? |
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Definition
GI: increased fluid secretion and peristalsis (diarrhea or vomiting)
Airways: decreased diameter and increased mucus secretion (phlegmatic cough) |
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Term
| What happens to blood vessels in mast cell degranulation? |
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Definition
| They dilate and become permeable, leading to edema, inflammation, and more lymph flow |
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Term
| How do activated mast cells signal B-cells to release IgE? |
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Definition
| CD40 contact and IL-4 secretion results in positive feedback |
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Term
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Definition
| Granulocytes that respond to parasitic infections by releasing toxic proteins |
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Term
| What is the major basic protein (MBP) and why is it used? |
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Definition
| MBP causes degranulation of mast cells that leads to recognition and death of parasites and the host. Hypereosinophila can lead to normal tissue damage |
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Term
| What other factors are secreted by eosinophils? |
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Definition
| LKTs and cytokines like IL-3 and IL-5 |
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