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

Publication Date


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.


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

DOI of Published Version



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

Journal/Book/Conference Title

Journal of leukocyte biology

PubMed ID