Abstract
Abstract Th17 cells have quickly become a paradigm of intense research interest, owing in part to their central role in mediating tissue-immune system communication, their demonstrable anti-tumor capacity, and their involvement in the pathogenesis of several autoimmune disorders. As with other effector Th1 and Th2 cells, they are members of a lineage derived from CD4 naïve cells, differentiating from their progenitors in response to immunological need. Recent research has revealed that differentiation of memory T-cells is dependent on the morphology of fluid mitochondrial networks, and in particular on remodeling dynamics that yield fused mitochondrial superstructures that favor oxidative phosphorylation-driven metabolism. In a similar fashion, our data suggest that Th17 T-cell differentiation is contingent upon highly fissed mitochondria network morphology, wherein a more independent arrangement of mitochondria and increased aerobic glycolsysis is employed. An important component of this research is the modulation of DRP-1, a GTPase that when phosphorylated in the cytosol initiates fission mitochondrial dynamics. Specifically, our data suggests that attenuation of DRP-1 action may play an important role in Th17 differentiation, and thus a better understanding of Th17 metabolism and how it affects immune cell fate, which at this time is poorly characterized.
Published Version
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