THE INDUCTION OF J11D ANTIGEN ON DOUBLE-NEGATIVE T-CELLS OF MRL MP-LPR/LPR MICE BY HIGH-DOSE CALCIUM IONOPHORE/

Mice homozygous for the lymphoproliferation (lpr) gene spontaneously d evelop autoimmune syndrome. These mice were characterized by the massi ve accumulation of double negative (DN) T cells. Although peripheral T cells in normal mice do not express J11d antigen, those abnormal DN T cells in autoimmune-prone mice express J11d antigen. In this study, t he mechanisms that control the expression of J11d antigen are analyzed . High concentration of calcium ionophore alone induces the expression of J11d antigen, but not of CD4. CD8, and activation antigens such as interleukin 2 receptor as well as transferrin receptor by J11d- DN T cells from lpr mice. The expression of J11d antigen is primarily regul ated at the transcription level rather t an t post transcription level . Experiments using metabolic inhibitors reveal that the induction of J11d antigen requires the activation of not only a Ca2+/calmodulin- bu t also protein kinase C-dependent signaling pathway. Furthermore, J11d - DN thymocytes from control mice share the similar functional propert y with DN lpr T cells in J11d antigen inducibility.