The role of the STING signaling pathway in the regulation of Th17 cell pathogenicity and its implication for autoimmunity

Abstract

Nucleic acids are essential carriers of genetic information of living organisms, however, it is known that tissue damage and cell death may result in release of DNA fragments, which in turn may directly activate the immune response. In this context, the adaptor protein STING (STimulator of INterferon Genes) was reported to be an important intracellular sensor for foreign and self-cytoplasmic DNA that activates a range of transcriptional factors, including those involved in type I IFN production. Although STING is broadly described in innate immune cells, little is known about its role in lymphocytes. It is noticeable that Th17 cells mediate the development of different autoimmune disorders, nevertheless, the dynamics of their pathogenicity is still poorly understood. Unexpectedly, our preliminary results demonstrate that STING activation is able to reduce IL-17 expression and concomitantly, increasing IL-10 production by Th17 cells under optimal conditions of differentiation. Thus, this research project aims to evaluate the influence of the STING signaling pathway on generation and regulation of Th17 cell pathogenicity and its consequences for autoimmunity. (AU)