G
Gary S. Gray
Researcher at Harvard University
Publications - 116
Citations - 14982
Gary S. Gray is an academic researcher from Harvard University. The author has contributed to research in topics: T cell & CD28. The author has an hindex of 56, co-authored 116 publications receiving 14756 citations. Previous affiliations of Gary S. Gray include Repligen Corporation & June.
Papers
More filters
Journal ArticleDOI
Cloning of B7-2: A CTLA-4 counter-receptor that costimulates human T cell proliferation
Gordon J. Freeman,John G. Gribben,Vassiliki A. Boussiotis,Judy W. Ng,Vincent A. Restivo,Lisa A. Lombard,Gary S. Gray,Lee M. Nadler +7 more
TL;DR: A counter-receptor of CD28 and CTLA-4 is cloned, termed B7-2, which also costimulates IL-2 production and T cell proliferation and is likely to provide a critical early costimulatory signal determining if the T cell will contribute to an immune response or become anergic.
Journal ArticleDOI
CTLA4-Ig and anti-CD40 ligand prevent renal allograft rejection in primates
Allan D. Kirk,David M. Harlan,Nicholas Armstrong,Thomas A. Davis,Yinchen Dong,Gary S. Gray,Xuening Hong,David Thomas,John H. Fechner,Stuart J. Knechtle +9 more
TL;DR: It is concluded that CTLA4-Ig and 5C8 can both prevent and reverse acute allografted rejection, significantly prolonging the survival of major histocompatibility complex-mismatched renal allografts in primates without the need for chronic immunosuppression.
Journal ArticleDOI
Inhibition of angiogenesis by recombinant human platelet factor-4 and related peptides.
Theodore E. Maione,Gary S. Gray,Joan Petro,Anthony J. Hunt,Amy L. Donner,Susan I. Bauer,Helen F. Carson,Richard J. Sharpe,Richard J. Sharpe +8 more
TL;DR: Recombinant human platelet factor-4 (rhPF4), purified from Escherichia coli, inhibited blood vessel proliferation in the chicken chorioallantoic membrane in a dose-dependent manner and suggested that the angiostatic effect was due to specific inhibition of growth factor-stimulated endothelial cell proliferation.
Journal ArticleDOI
Differential effects of anti-B7-1 and anti-B7-2 monoclonal antibody treatment on the development of diabetes in the nonobese diabetic mouse.
Deborah J. Lenschow,Stephen C. Ho,I Husain Sattar,Lesley Rhee,Gary S. Gray,S Nasrin Nabavi,Kevan C. Herold,Jeffrey A. Bluestone +7 more
TL;DR: Results suggest that blockade of costimulatory signals by CTLA4Ig or anti-B7-2 acts early in disease development, after insulitis but before the onset of frank diabetes, and that different members of the B7 family have distinct regulatory functions during the development of autoimmune diabetes.
Journal ArticleDOI
Human T-cell clonal anergy is induced by antigen presentation in the absence of B7 costimulation.
TL;DR: In a human antigen-specific model system, when tetanus toxoid peptide antigen is presented by cells cotransfected with HLA-DR7 and B7, optimal T-cell proliferation and interleukin 2 production result, demonstrating that it is possible to induce antigen- specific clonal tolerance in human T cells that have been previously sensitized to antigen.