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Complete expression of the human immune response requires the generation of activated T cells1. This activation sequence is initiated by an interaction of antigen with specific receptors present on the membrane of resting T cells. This receptor-ligand interaction, in the presence of macrophage derived interleukin-1 (IL-1), then triggers the production of interleukin-2 (IL-2, previously designated T cell growth factor)2,3. IL-2 is a well-characterized 14,500 dalton glycoprotein which promotes T cell proliferation following binding to specific high affinity IL-2 membrane receptors4–6. However, unlike receptors for antigen, IL-2 receptors are not expressed by resting T cells, but like IL-2, are synthesized following antigen activation. The interaction of IL-2 with its inducible receptor results in T cell proliferation and expansion of the antigen reactive T cell clone and culminates in the emergence of T cells mediating helper, suppressor, and cytotoxic T cell function. Thus, both the specificity and magnitude of the T cell immune response is in large measure controlled at the level of IL-2 receptor expression. |
