MHC class I molecules on CD4 T cells regulate receptor-mediated activationsignals

Three T cell populations can be distinguished based on their response to an tigen receptor engagement. A sizable fraction dies within hours of TCR liga tion, a smaller fraction enters the mitotic cycle, and the remaining T cell s merely upregulate the expression of certain cell surface markers. An MHC- I-controlled regulatory mechanism has been identified. MHC I MAbs, or Fab f ragments, prevent T cells from mounting a proliferative mitogen response bu t do not inhibit the mitogen-induced deletion of T cells. IFN-gamma enlarge s the fraction of T cells which proliferate in response to mitogen stimulat ion but, in the presence of MHC I MAb, these cells fail to clonally expand and enter the deletion pathway. Phenotypically, MHC I MAb Fab fragments ind uce T cells to upregulate the expression of the apoptosis marker CD95, even in the absence of TCR ligand, and prevent the upregulation of costimulator y CD28 molecule expression, (C) 1999 Academic Press.