Affordable Access

Publisher Website

T Cell Costimulation through CD28 Depends on Induction of the Bcl-xγ Isoform : Analysis of Bcl-xγ–deficient Mice

Authors
Journal
Journal of Experimental Medicine
0022-1007
Publisher
The Rockefeller University Press
Publication Date
Volume
196
Issue
1
Identifiers
DOI: 10.1084/jem.20012084
Keywords
  • Article
Disciplines
  • Biology

Abstract

The molecular basis of CD28-dependent costimulation of T cells is poorly understood. Bcl-xγ 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-xγ–deficient (Bcl-xγ−/−) 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-xγ largely replaces the requirement for B7-dependent ligation of CD28. These findings identify the Bcl-xγ cytosolic protein as an essential downstream link in the CD28-dependent signaling pathway that underlies T cell costimulation.

There are no comments yet on this publication. Be the first to share your thoughts.