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Context-dependent regulation of Th17-associated genes and IFNγ expression by the transcription factor NFAT5. Context-dependent regulation of Th17-associated genes and IFNγ expression by the transcription factor NFAT5. M. Alberdi, M. Iglesias, S. Tejedor, R. Merino, C. López-Rodríguez and J. Aramburu. 2016-09-05T22:00:00Z<p>​<strong class="ms-rteFontSize-2" style="text-align:justify;">Abstract:</strong></p><p style="text-align:justify;"><span class="ms-rteFontSize-2">Stress-activated transcription factors influence T-cell function in different physiopathologic contexts. NFAT5, a relative of nuclear factor κB and the calcineurin-activated NFATc transcription factors, protects mammalian cells from hyperosmotic stress caused by the elevation of extracellular sodium levels. In T cells exposed to hypernatremia, NFAT5 not only induces osmoprotective gene products but also cytokines and immune receptors, which raises the question of whether this factor could regulate other T-cell functions in osmostress-independent contexts. Here we have used mice with a conditional deletion of Nfat5 in mature T lymphocytes to explore osmostress-dependent and -independent functions of this factor. In vitro experiments with CD4 T cells stimulated in hyperosmotic medium showed that NFAT5 enhanced the expression of IL-2 and the Th17-associated gene products RORγt and IL-23R. By contrast, NFAT5-deficient CD4 T cells activated in vivo by anti-CD3 antibody exhibited a different activation profile and were skewed towards enhanced interferon γ(IFNγ) and IL-17 expression and attenuated Treg responses. Using a model of experimental colitis, we observed that mice lacking NFAT5 in T cells exhibited exacerbated intestinal colitis and enhanced expression of IFNγin draining lymph nodes and colon. These results show that NFAT5 can modulate different T-cell responses depending on stress conditions and stimulatory context.</span><br></p><p><a href="https://onlinelibrary.wiley.com/doi/full/10.1038/icb.2016.69">​Immunol. Cell Biol. 2017, 95:56-67. doi: 10.1038/icb.2016.69.</a><br></p>169

 
IBBTEC

Instituto de Biomedicina y Biotecnología de Cantabria.
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