Journal
IMMUNITY
Volume 21, Issue 6, Pages 781-791Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2004.10.008
Keywords
-
Categories
Funding
- NIAID NIH HHS [AI53091-01, R01 AI053091, R01 AI053091-01] Funding Source: Medline
- NIDDK NIH HHS [T32 DK007233-28, T32 DK007233, 5T32DK07233] Funding Source: Medline
Ask authors/readers for more resources
DRAK2 is a member of the death-associated protein (DAP)-like family of serine/threonine kinases. Members of this family induce apoptosis in various cell types. DRAK2, in particular, is specifically expressed in T cells and B cells, and it is differentially regulated during T cell development. To determine whether DRAK2 regulates lymphocyte apoptosis, we produced Drak2(-1-) mice. Contrary to our expectations, Drak2(-/-) T cells did not demonstrate any defects in apoptosis or negative selection; however, T cells from Drak2-1mice exhibited enhanced sensitivity to T cell receptor-mediated stimulation with a reduced requirement for costimulation. These results provide evidence that DRAK2 raises the threshold for T cell activation by negatively regulating signals through the TCR. In contrast to other models of T cell hypersensitivity, Drak2-1mice were remarkably resistant to experimental autoimmune encephalomyelitis (EAE). These results expose a new pathway regulating T cell activation and highlight the intricacies of induced autoimmune disease.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available