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Sudesh Pawaria, Shruti Sharma, Rebecca Baum, Kerstin Nündel, Patricia Busto, Ellen M Gravallese, Katherine A Fitzgerald, Ann Marshak-Rothstein, Taking the STING out of TLR-driven autoimmune diseases: good, bad, or indifferent?, Journal of Leukocyte Biology, Volume 101, Issue 1, Jan 2017, Pages 121–126, https://doi.org/10.1189/jlb.3MR0316-115R
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Abstract
Both endosomal and cytosolic-nucleic acid–sensing receptors can detect endogenous ligands and promote autoimmunity and autoinflammation. These responses involve a complex interplay among and between the cytosolic and endosomal sensors involving both hematopoietic and radioresistant cells. Cytosolic sensors directly promote inflammatory responses through the production of type I IFNs and proinflammatory cytokines. Inflammation-associated tissue damage can further promote autoimmune responses indirectly, as receptor-mediated internalization of the resulting cell debris can activate endosomal Toll-like receptors (TLR). Both endosomal and cytosolic receptors can also negatively regulate inflammatory responses. A better understanding of the factors and pathways that promote and constrain autoimmune diseases will have important implications for the development of agonists and antagonists that modulate these pathways.
