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Interleukin 2 (IL-2)-deficient (IL-2(-/-)) mice develop hemolytic anemia and chronic inflammatory bowel disease. Importantly, the induction of disease in IL-2-deficient mice is critically dependent on CD4+ T cells. We have studied the requirements of T cells from IL-2-deficient mice for costimulation with B7 antigens. Stable B7-1 or B7-2 chinese hamster ovary (CHO) cell transfectants could synergize with anti-CD3 monoclonal antibody (mAb) to induce the proliferation of CD4+ T cells from IL2(-/-) mutant mice. Further mechanistic studies established that B7-induced activation resulted in surface expression of the α chain of the IL-2 receptor. B7-induced proliferation occurred independently of IL-4 and was largely independent of the common γ chain of the IL-2, IL-4, IL-7, IL-9, and IL-15 receptors. Finally, anti-B7-2 but not anti-B7-1 mAb was able to inhibit the activation of IL-2(-/-) T cells induced by anti-CD3 mAb in the presence of syngeneic antigen-presenting cells. The results of our experiments indicate that IL- 2(-/-) CD4+ T cells remain responsive to B7 stimulation and raise the possibility that B7 antagonists have a role in the prevention/treatment of inflammatory bowel disease.

Original publication

DOI

10.1073/pnas.93.7.2903

Type

Journal article

Journal

Proceedings of the National Academy of Sciences of the United States of America

Publication Date

02/04/1996

Volume

93

Pages

2903 - 2908