منابع مشابه
ICER is requisite for Th17 differentiation
Inducible cAMP early repressor (ICER) has been described as a transcriptional repressor isoform of the cAMP response element modulator (CREM). Here we report that ICER is predominantly expressed in Th17 cells through the IL-6-STAT3 pathway and binds to the Il17a promoter, where it facilitates the accumulation of the canonical enhancer RORγt. In vitro differentiation from naive ICER/CREM-deficie...
متن کاملIRAK4 kinase activity is required for Th17 differentiation and Th17-mediated disease.
Both IL-23- and IL-1-mediated signaling pathways play important roles in Th17 cell differentiation, cytokine production, and autoimmune diseases. The IL-1R-associated kinase 4 (IRAK4) is critical for IL-1/TLR signaling. We show here that inactivation of IRAK4 kinase in mice (IRAK4 KI) results in significant resistance to experimental autoimmune encephalomyelitis due to a reduction in infiltrati...
متن کاملEts-1 is a negative regulator of Th17 differentiation
IL-17 is a proinflammatory cytokine that plays a role in the clearance of extracellular bacteria and contributes to the pathology of many autoimmune and allergic conditions. IL-17 is produced mainly by a newly characterized subset of T helper (Th) cells termed Th17. Although the role of Th17 cells in the pathology of autoimmune diseases is well established, the transcription factors regulating ...
متن کاملCytokine regulation of Th17 differentiation
Introduction The random rearrangement of adaptive antigen receptors allows for incredible diversity of antigen receptor specificity but comes at the cost of creating potentially autoreactive T and B lymphocytes. Although many potentially autoreactive clones are deleted during development or are prevented from causing disease by the various mechanisms of peripheral tolerance, others go on to ind...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Nature Communications
سال: 2016
ISSN: 2041-1723
DOI: 10.1038/ncomms12993