Transcriptional regulation of the mucosal immune system mediated by T-bet
Author:
Publisher
Springer Science and Business Media LLC
Subject
Immunology,Immunology and Allergy
Link
http://www.nature.com/articles/mi201053.pdf
Reference123 articles.
1. Szabo, S.J., Kim, S.T., Costa, G.L., Zhang, X., Fathman, C.G. & Glimcher, L.H. A novel transcription factor, T-bet, directs Th1 lineage commitment. Cell 100, 655–669 (2000).
2. Esensten, J.H., Lee, M.R., Glimcher, L.H. & Bluestone, J.A. T-bet-deficient NOD mice are protected from diabetes due to defects in both T cell and innate immune system function. J. Immunol. 183, 75–82 (2009).
3. Bettelli, E., Sullivan, B., Szabo, S.J., Sobel, R.A., Glimcher, L.H. & Kuchroo, V.K. Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis. J. Exp. Med. 200, 79–87 (2004).
4. Peng, S.L., Szabo, S.J. & Glimcher, L.H. T-bet regulates IgG class switching and pathogenic autoantibody production. Proc. Natl Acad. Sci. USA 99, 5545–5550 (2002).
5. Neurath, M.F. et al. The transcription factor T-bet regulates mucosal T cell activation in experimental colitis and Crohn's disease. J. Exp. Med. 195, 1129–1143 (2002).
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