Contingent genetic regulatory events in T lymphocyte activation.
Interaction of antigen in the proper histocompatibility context with the T lymphocyte antigen receptor leads to an orderly series of events resulting in morphologic change, proliferation, and the acquisition of immunologic function. In most T lymphocytes two signals are required to initiate this process, one supplied by the antigen receptor and the other by accessory cells or agents that activate protein kinase C. Recently, DNA sequences have been identified that act as response elements for one or the other of the two signals, but do not respond to both signals. The fact that these sequences lie within the control regions of the same genes suggests that signals originating from separate cell membrane receptors are integrated at the level of the responsive gene. The view is put forth that these signals initiate a contingent series of gene activations that bring about proliferation and impart immunologic function.
Department of Pathology, Stanford University Medical School, CA.
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Crabtree
D000818:Animals; D005786:Gene Expression Regulation; D006801:Humans; D007376:Interleukin-2 / Q000235:genetics; D008213:Lymphocyte Activation; D051379:Mice; D009857:Oncogenes; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D013601:T-Lymphocytes / Q000502:physiology*; D013997:Time Factors
D007376:Interleukin-2; D011505:Protein-Tyrosine Kinases