The transcriptional coactivator TAZ regulates reciprocal differentiation of TH17 cells and Treg cells


Regulatory T cells (Treg) and TH17 lymphocytes are, no doubt, crucial players in the course and outcome of inflammatory events, and their unbalance is suspected to be a major culprit in triggering many chronic and autoimmune conditions.

Given their pivotal role in shaping immune responses, their development is finely orchestrated by the action of several cytokines. TGF-beta works by inducing both Treg and TH17 signature transcription factors (i.e. FoxP3 and RORgt, respectively), although, in order to trigger the develompment of TH17 phenotype, it needs to work alongside other cytokines (e.g. IL23, IL1-beta). The concerted action of these factors triggers STAT3 pathway that, in turn, suppresses Treg features while promoting proper TH17 phenotype. However the details behind this mechanism are still largely unknown.

In this month’s issue of Nature Immunology, Jing Geng et al. unveiled an important piece of the convoluted puzzle that is the molecular network that oversees the balance between Treg and TH17 function. According to the paper, the protein TAZ, which belongs to the Hippo pathway, is required for TH17 differentiation and phlogistic functions in inflammatory and autoimmune diseases.

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