C1.7 MONOCLONAL-ANTIBODY DESIGNATES HIGH-AVIDITY CD4(-LYMPHOCYTES INVOLVED IN CLINICAL HEART REJECTION() CYTOTOXIC T)

Background, It is assumed that not all donor-specific cytotoxic T lymp hocytes (CTLs), but only those with a high avidity for donor antigens, can function as terminal effector cells in transplant rejection, Meth ods. In the present study, we searched for markers that would exclusiv ely designate these high-avidity CTL, Results. FAGS analysis of donor- specific CTL clones obtained from heart transplant patients revealed t hat high- and low-avidity CTL varied in their expression of p38, a sur face molecule involved in signal transduction, which is stained by the antibody C1.7. High- and tow-avidity CD8(+) CTL and high-avidity CD4( +) CTL expressed p38, whereas low-avidity CD4(+) CTL did not, Noncytot oxic and naive CD4(+) lymphocytes also lacked p38 surface expression. Conclusion. Therefore, we conclude that p38 is a marker for CD4(+) lym phocytes with the potency to damage the transplanted heart. Accordingl y, p38 might be used to analyze the contribution of CD4(+) CTL in immu ne responses, such as transplant rejection.