MHC class I molecules on CD4 T cells regulate receptor-mediated activation signals.
Three T cell populations can be distinguished based on their response to antigen receptor engagement. A sizable fraction dies within hours of TCR ligation, a smaller fraction enters the mitotic cycle, and the remaining T cells merely upregulate the expression of certain cell surface markers. An MHC-I-controlled regulatory mechanism has been identified. MHC I MAbs, or Fab fragments, prevent T cells from mounting a proliferative mitogen response but do not inhibit the mitogen-induced deletion of T cells. IFN-gamma enlarges the fraction of T cells which proliferate in response to mitogen stimulation 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 induce T cells to upregulate the expression of the apoptosis marker CD95, even in the absence of TCR ligand, and prevent the upregulation of costimulatory CD28 molecule expression.
Wang
Z Q
ZQ
Department of Microbiology and Immunology, New York Medical College, Valhalla, New York, 10595, USA.
Bapat
A S
AS
Trejo
V
V
Orlikowsky
T
T
Mittler
R S
RS
Hoffmann
M K
MK
D000911:Antibodies, Monoclonal / Q000276:immunology; D017209:Apoptosis; D018106:CD28 Antigens / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000502:physiology*; D006801:Humans; D008213:Lymphocyte Activation; D011948:Receptors, Antigen, T-Cell / Q000502:physiology*; D019014:fas Receptor / Q000032:analysis
D000911:Antibodies, Monoclonal; D018106:CD28 Antigens; D015395:Histocompatibility Antigens Class I; D011948:Receptors, Antigen, T-Cell; D019014:fas Receptor