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10.1016/j.clim.2015.04.004

http://scihub22266oqcxt.onion/10.1016/j.clim.2015.04.004
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C4465043!4465043!25869298
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suck abstract from ncbi


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pmid25869298      Clin+Immunol 2015 ; 158 (2): 221-30
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  • Signal Transducer and Activator of Transcription (STAT) 3 Inhibition Delays The Onset Of Lupus Nephritis In MRL/lpr Mice #MMPMID25869298
  • Edwards LJ; Mizui M; Kyttaris V
  • Clin Immunol 2015[Jun]; 158 (2): 221-30 PMID25869298show ga
  • The transcription factor STAT3 is overexpressed and hyperactivated in T cells from SLE patients. STAT3 plays a central role in T cell differentiation into Th17 and T follicular helper cells, two subsets that orchestrate autoimmune responses in SLE. Moreover, STAT3 is important in chemokine-mediated T cell migration. To better understand its role in SLE, we inhibited STAT3 in lupus-prone mice using the small molecule Stattic. Stattic-treated mice exhibited delayed onset of proteinuria (3 weeks later than controls), and had lower levels of anti-dsDNA antibodies and inflammatory cytokines. Inhibitor treatment reduced lymphadenopathy, resulted in a 3-fold decrease in total T cell number, and a 4-fold decrease in the numbers of T follicular helper cells. In vitro experiments showed that Stattic-treated T cells exhibited decreased proliferation and a decrease in ability to migrate to CXCL12. We propose that STAT3 inhibition represents a therapeutic target in SLE, particularly lupus nephritis.
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