The Immune Response
- First, macrophages phagocytose antigen and
present fragments complexed to the Class II MHC glycoprotein to T- cells.
- The EM picture shows a macrophage attempting
to ingest an asbestos particle.
- Helper (CD4)T-cells with receptor recognizing both antigen and the Class
II cause the macrophage to produce growth stimulatory cytokines which in turn cause
a clonal expansion of the T-cell.
- Previous selection in the thymus insures that clones of T-cells capable of
reacting with self peptides are eliminated.
- Receptor on the T-cell binds to both antigen fragment and Class II MHC.
- B-cells have IgM as a cell membrane receptor. The antigen binds to a B-cell
clone with the correct antibody and is then endocytosed and degraded with fragments
binding to Class II MHC on the cell surface.
- Recognition of this complex by the expanded clone of Helper T-cells
produces cytokines to stimulate B-cell proliferation and differentiation.
Cytotoxic T-cells
Selection of cytotoxic T-cells also requires T-helper cells. Killing requires
dual recognition of class I MHC complexed with non-self peptides. Self reactive
T-cells die in the thymus.
MHC regulation
- Probably prevents autoimmune disease.
- T-cell receptors on CD4 and CD8 T-cells are diverse as the antibodies and also
arise by gene rearrangement.
- Thymus- selection for T-cells with receptors specific for our own MHC but not
reacting with our own peptides.
- Diversity of MHC within a species is needed since the biological recognition
requires a complex between MHC and abnormal protein fragments.
- If we are all different, then we are more likely to be able to fight any new kind
of pathogen that appears.
Allergy- mast cells bind IgE and upon antigen recognition cause the release
of histamines. The most serious allergic reactions trigger anaphylatic shock.
wjgrimes@u.arizona.edu
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