Journal
SCIENCE
Volume 303, Issue 5660, Pages 1017-1020Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1093889
Keywords
-
Categories
Funding
- NHLBI NIH HHS [HL56244, HL63988] Funding Source: Medline
- NIAID NIH HHS [AI057471, AI01803] Funding Source: Medline
- NIDDK NIH HHS [DK52574] Funding Source: Medline
Ask authors/readers for more resources
Forkhead transcription factors play key roles in the regulation of immune responses. Here, we identify a role for one member of this family, Foxj1, in the regulation of T cell activation and autoreactivity. Foxj1 deficiency resulted in multiorgan systemic inflammation, exaggerated Th1 cytokine production, and T cell proliferation in autologous mixed lymphocyte reactions. Foxj1 suppressed NF-kappaB transcription activity in vitro, and Foxj1-deficient T cells possessed increased NF-kappaB activity in vivo, correlating with the ability of Foxj1 to regulate IkappaB proteins, particularly IkappaBbeta. Thus, Foxj1 likely modulates inflammatory reactions and prevents autoimmunity by antagonizing proinflammatory transcriptional activities. These results suggest a potentially general role for forkhead genes in the enforcement of lymphocyte quiescence.
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