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* Diabetes Center and Department of Medicine, University of California, San Francisco, CA 94143;
Deparment of Rheumatology, Children’s Hospital Medical Center, Cincinnati, OH 45229;
Department of Surgery, Section of Transplantation and
Department of Medicine, Section of Rheumatology, University of Chicago, Chicago, IL 60637;
¶ Abramson Research Institute, University of Pennsylvania Cancer Center, Philadelphia, PA 19104
FcR-binding "classical" anti-CD3 mAb is a potent immunosuppressive drug that alters CD4+ and CD8+ T cell function in vivo via anergy induction and programmed cell death (PCD). Anti-CD3-mediated PCD was Fas independent but was mediated by the mitochondria-initiated apoptosis that was abrogated in Bcl-xL-transgenic T cells. The PCD was more pronounced in CD28-deficient mice consistent with defective Bcl-xL up-regulation. Residual T cells isolated from anti-CD3-treated wild-type, CD28-/-, and Bcl-xL-transgenic mice were hyporesponsive. The hyporesponsiveness was more pronounced in CD28-/- and wild-type mice treated with anti-B7-2, suggesting that CD28 interaction with B7-2 regulates T cell responsiveness in anti-CD3-treated animals. Finally, anti-CD3 treatment led to indefinite cardiac allograft survival in wild-type but not Bcl-xL animals. Together these results implicate CD28/B7 signaling in the regulation of both anti-CD3-induced T cell depletion and hyporesponsiveness in vivo, but T cell depletion, not hyporesponsiveness, appears to be critical for anti-CD3 mAb-mediated long-term immune regulation.
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