INVOLVEMENT OF P21(RAS) ACTIVATION IN T-CELL CD69 EXPRESSION

The involvement of p21(ras) in the induction of the early activation a ntigen CD69 was investigated in T cells. Expression of a v-Ha-ras codi ng for a constitutively active ras protein in Jurkat cells resulted in CD69 induction on the cell surface. Transfected ras was shown to be c onstitutively activated and functionally efficient, since it could be immunoprecipitated in the guanosine triphosphate (GTP)-bound form and it induced transactivation of an AP-1 consensus-chloramphenicol acetyl transferase reporter gene. The requirement for ras activation in T cel l receptor (TcR) CD3-mediated CD69 induction was also investigated. Th e expression of a dominant negative c-Ha-ras-N17 mutant markedly reduc ed the amount of GTP that could be immunoprecipitated from ras protein s after TcR/CD3 triggering in Jurkat cells, and concomitantly decrease d TcR/CD3-mediated CD69 induction. These results suggest a central rol e for ras in TcR/CD3-mediated CD69 expression in T cells.