| Literature DB >> 19100630 |
Yongmei Wang1, J T Evans, Frederick Rodriguez, Patrick Fields, Cynthia Mueller, Tanuja Chitnis, Samia J Khoury, Margaret S Bynoe.
Abstract
T helper 2 (Th2) cytokines are known to be important in protection against experimental autoimmune encephalomyelitis (EAE). To investigate the role of the signal transducer and activator of transcription factor 6 (STAT6) in EAE we used mice with two different targeted disruptions of the STAT6 gene. In this report, we show that mice with a targeted deletion of the first coding exon of the SH2 domain of STAT6 induce Th2 cell differentiation and are resistant to EAE induction. By contrast, STAT6(-/-) mice generated by deletion of amino acids 505 to 584 encoding the SH2 domain of STAT6 are defective in Th2 cell differentiation and develop very severe EAE. These results suggest that an altered STAT6 gene can be more efficient than wild type STAT6 in regulating the autoimmune response in EAE.Entities:
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Year: 2008 PMID： 19100630 PMCID： PMC2762219 DOI： 10.1016/j.jneuroim.2008.11.003
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478