SIGNALING BY A NEW ANTI-THY-1 MONOCLONAL-ANTIBODY INHIBITS T-CELL PROLIFERATION AND INTERFERES WITH T-CELL-MEDIATED INDUCTION OF COSTIMULATORY MOLECULE B7-2

被引:8
作者
WU, Y
GUO, Y
JANEWAY, CA
LIU, Y
机构
[1] NYU, MED CTR, DEPT PATHOL, MICHAEL HEIDELBERGER DIV IMMUNOL, NEW YORK, NY 10016 USA
[2] NYU, MED CTR, KAPLAN COMPREHENS CAN CTR, NEW YORK, NY 10016 USA
[3] YALE UNIV, SCH MED, IMMUNOBIOL SECT, NEW HAVEN, CT 06520 USA
[4] HOWARD HUGHES MED INST, NEW HAVEN, CT 06510 USA
关键词
D O I
10.1006/cimm.1995.1213
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Costimulatory activity on antigen-presenting cells is a critical determinant of the fate T cells when the T cell receptors are engaged by MHC:peptide complexes. Therefore, control of the expression of the costimulatory molecules regulates T cell responses. While several types of interactions between T cells and B cells up-regulate costimulatory molecules on antigen-presenting cell, no T cell surface molecules have been implicated in inhibiting the induction of the costimulatory molecules on B cells. Here we characterize a new anti-Thy1 mAb, 21F10, which inhibits T cell proliferation to selective stimuli. T cells stimulated by anti-CD3 together with anti-Thy1 mAb are anergic to further stimulation through the CD3, which suggests that the anti-Thy1 mAb interferes with the delivery of the costimulatory activity to T cells. Consistent with this notion, anti-Thy1 mAb 21F10 completely inhibits the induction of B7-2 on B cells. Induction of several T cell surface molecules such as CD69 and CD40 ligand was largely unaffected. As this inhibition requires a bivalent anti-Thy1 mAb and does not require binding of more than 50% of Thy1 molecules on T cell surface, we suggest that Thy1 may mediate a negative signaling pathway which inhibits the T-cell-mediated induction of costimulatory activity, including expression of costimulatory molecule B7-2. (C) 1995 Academic Press, Inc.
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页码:266 / 277
页数:12
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