University of Massachusetts Medical School Faculty Publications


Taking the STING out of TLR-driven autoimmune diseases: good, bad, or indifferent

UMMS Affiliation

Department of Medicine, Division of Rheumatology; Department of Medicine, Division of Infectious Diseases and Immunology; Program in Innate Immunity



Document Type



Cell Biology | Immune System Diseases | Immunology and Infectious Disease


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.

Rights and Permissions

Citation: J Leukoc Biol. 2017 Jan;101(1):121-126. doi: 10.1189/jlb.3MR0316-115R. Epub 2016 Aug 16. Link to article on publisher's site

Related Resources

Link to Article in PubMed


Toll-like receptor, autoantibody, cGAS, systemic lupus erythematosus

PubMed ID