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.
journal_name
J Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Wang Y,Evans JT,Rodriguez F,Fields P,Mueller C,Chitnis T,Khoury SJ,Bynoe MSdoi
10.1016/j.jneuroim.2008.11.003subject
Has Abstractpub_date
2009-01-03 00:00:00pages
76-85issue
1-2eissn
0165-5728issn
1872-8421pii
S0165-5728(08)00480-3journal_volume
206pub_type
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