Insulin modulates the interleukin 2 responsiveness of T lymphocytes.
Insulin has been shown to enhance the proliferation and differentiation of T cells stimulated by both polyclonal stimulants and specific antigen. This study describes an experimental system designed to understand the mechanism(s) by which occupancy of the insulin receptor mediates the enhancement seen in T cell expansion. These experiments demonstrate that the ability of insulin to influence T cell expansion resides in an insulin-mediated maintenance of the interleukin-2 (IL-2) responsiveness of the activated cells. This was analyzed by following the decay pattern of T cell IL-2 responsiveness by placing the activated T cells into serum-free cultures in the presence or absence of insulin. This maintenance of responsiveness was not mediated by insulin regulating the expression of the IL-2 receptor alpha chain. We feel that this experimental approach will prove useful for dissecting the biochemical and molecular changes mediated by insulin which interface with the ability of activated T cells to effectively respond to IL-2.
DeBenedette
M
M
Department of Microbiology and Immunology, University of Kentucky Medical Center, Lexington 40536-0084.
Snow
E C
EC
D000818:Animals; D002478:Cells, Cultured; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007328:Insulin / Q000494:pharmacology*; D007376:Interleukin-2 / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D051379:Mice; D008811:Mice, Inbred DBA / Q000276:immunology; D051381:Rats; D011972:Receptor, Insulin / Q000096:biosynthesis / Q000502:physiology; D013268:Stimulation, Chemical; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects*
D007328:Insulin; D007376:Interleukin-2; D011972:Receptor, Insulin