Sensors of the innate immune system: Their link to rheumatic diseases

Argyrios N. Theofilopoulos, Rosana Gonzalez-Quintial, Brian R. Lawson, Yi T. Koh, Michael E. Stern, Dwight H. Kono, Bruce Beutler, Roberto Baccala

Research output: Contribution to journalReview articlepeer-review

66 Scopus citations


Evidence strongly suggests that excessive or protracted signaling, or both, by cell-surface or intracellular innate immune receptors is central to the pathogenesis of most autoimmune and autoinflammatory rheumatic diseases. The initiation of aberrant innate and adaptive immune responses in autoimmune diseases can be triggered by microbes and, at times, by endogenous molecules-particularly nucleic acids and related immune complexes-under sterile conditions. By contrast, most autoinflammatory syndromes are generally dependent on germline or de novo gene mutations that cause or facilitate inflammasome assembly. The consequent production of proinflammatory cytokines, principally interferon-α/Β and tumor necrosis factor in autoimmune diseases, and interleukin-1Β in autoinflammatory diseases, leads to the creation of autoamplification feedback loops and chronicity of these syndromes. These findings have resulted in a critical reappraisal of pathogenetic mechanisms, and provide a basis for the development of novel diagnostic and therapeutic modalities for these diseases.

Original languageEnglish (US)
Pages (from-to)146-156
Number of pages11
JournalNature Reviews Rheumatology
Issue number3
StatePublished - Mar 2010

ASJC Scopus subject areas

  • Rheumatology


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