THE INDUCTION OF Jlld ANTIGEN ON DOUBLE NEGATIVE CALCIUM IONOPHORE T CELLS OF MRLIMp-LPRILPR MICE BY HIGH DOSE

Mice homozygous for the lymphoproliferation (Ipr) gene spontaneously develop autoimmune syndrome. These mice were characterized by the massive accumulation of double negative (DN) T cells. Although peripheral T cells in normal mice do not express J1 Id antigen, those abnormal DN T cells in autoimmune-prone mice express J1 Id antigen. In this study, the mechanisms that control the expression of J1 Id antigen are analyzed. High concentration of calcium ionophore alone induces the expression of J1 Id antigen, but not of CD4. CDS, and activation antigens such as interleukin 2 receptor as well as transfemn receptor by J1 Id- DN T cells from Ipr mice. The expression of JI Id antigen is primarily regulated at the transcription level rather than the post transcription level. Experiments using metabolic inhibitors reveal that the induction of J1 Id antigen requires the activation of not only a Caz*/calmodulin- but also protein kinase C-dependent signaling pathway. Furthermore, J1 Id- DN thymocytes from control mice share the similar functional property with DN Ipr T cells in J1 Id antigen inducibility.

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