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T Cell Costimulatory Blockade

New Therapies for TransplantRejection

Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Correspondence to Dr. Laurence A. Turka, University of Pennsylvania, 901 Stellar-Chance Laboratories, 422 Curie Boulevard, Philadelphia, PA 19104-6100. Phone: 215-898-1018; Fax: 215-573-2880; E-mail: turka{at}mail.med.upenn.edu

Abstract

Abstract. Optimal T cell responses occur when T cells receive both antigen-specific signals through the T cell receptor and non-antigen-specific costimulatory signals through accessory cell surface molecules. The best understood costimulatory receptor is CD28. Signals through the T cell receptor and CD28 cooperatively induce cytokine gene expression and promote T cell proliferation and survival. Negative signals delivered through a related cell surface receptor, cytotoxic T lymphocyte antigen (CTLA-4), act to terminate immune responses and are required for normal immune homeostasis. This article reviews T cell costimulation, including the CD28/CTLA-4 system and other potential costimulatory pathways (such as CD40/CD154), the role of these pathways in normal immune responses, and the potential for the inhibition of these pathways to induce transplantation tolerance.

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