[Defect of TCR-mediated signal pathway of T cells in IDDM patients].
OBJECTIVE
To study the mechanism responsible for alteration of T cell response in IDDM patients.


METHODS
T cells from peripheral blood of IDDM patients were activated by anti-TCR antibodies. The level of TCR-mediated signaling pathway was analyzed.


RESULTS
T cells from IDDM patients responded weakly to anti-TCR antibody-induced proliferation, as compared with T cells from normal subjects (P < 0.05). The defect could be partially remedied by the addition of rIL-2, while the anti-CD28 antibody stimulation did not restore the proliferative response of anti-TCR-induced cells from IDDM patients (P = 0.03).


CONCLUSIONS
Unresponsiveness of the T cells from IDDM patients to anti-TCR antibody may result from a defect in the signaling pathway, the CD28 co-stimulation-signaling pathway is normal. Defect in the TCR signaling pathway increases the sensitivity of T cells from IDDM patients to apoptosis or anergy.
Li
Hong-mei
HM
Department of Clinical Laboratory, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Zhong
Ren-qian
RQ
Yu
Jia-ping
JP
Cao
Lu-ning
LN
Kong
Xian-tao
XT
Chen
Wei-feng
WF
D000911:Antibodies, Monoclonal / Q000276:immunology*; D018106:CD28 Antigens / Q000276:immunology; D049109:Cell Proliferation; D002478:Cells, Cultured; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008213:Lymphocyte Activation; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000911:Antibodies, Monoclonal; D018106:CD28 Antigens; D007376:Interleukin-2; D016693:Receptors, Antigen, T-Cell, alpha-beta; D015847:Interleukin-4; D013755:Tetradecanoylphorbol Acetate