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