The Journal of Experimental Medicine
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Published 1 July 2002. doi:10.1084/jem.20012084
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© Rockefeller University Press, 0022-1007/2002/7/87/ $5.00
The Journal of Experimental Medicine, Volume 196, Number 1, July 1, 2002 87-95

T Cell Costimulation through CD28 Depends on Induction of the Bcl-x{gamma} Isoform : Analysis of Bcl-x{gamma}–deficient Mice



Qunrui Ye1, Barry Press1, Stephan Kissler1, Xiao-Feng Yang1, Linrong Lu1, Craig H. Bassing2, Barry P. Sleckman2, Marianne Jansson1, Vily Panoutsakopoulou1, Linda A. Trimble1, Frederick W. Alt2 and Harvey Cantor1

1 Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, MA 02115
2 Department of Genetics, Harvard Medical School, Howard Hughes Medical Institute, Children's Hospital, and Center for Blood Research, Boston, MA 02115

Address correspondence to H. Cantor, Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, 44 Binney St., SM 722, Boston, MA 02115. Phone: 617-632-3348; Fax: 617-632-4630; E-mail: Harvey_Cantor{at}dfci.harvard.edu

The molecular basis of CD28-dependent costimulation of T cells is poorly understood. Bcl-x{gamma} is a member of the Bcl-x family whose expression is restricted to activated T cells and requires CD28-dependent ligation for full expression. We report that Bcl-x{gamma}–deficient (Bcl-x{gamma}-/-) T cells display defective proliferative and cytokine responses to CD28-dependent costimulatory signals, impaired memory responses to proteolipid protein peptide (PLP), and do not develop PLP-induced experimental autoimmune encephalomyelitis (EAE). In contrast, enforced expression of Bcl-x{gamma} largely replaces the requirement for B7-dependent ligation of CD28. These findings identify the Bcl-x{gamma} cytosolic protein as an essential downstream link in the CD28-dependent signaling pathway that underlies T cell costimulation.

Key Words: Bcl-x{gamma} • CD28 • T cell • costimulation • EAE


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