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Inflammasomes are multimeric cytosolic protein complexes that form to mediate host immune responses upon recognizing pathogen\u2010 or damage\u2010associated molecular patterns via pattern\u2010recognition receptors (\n                    <jats:styled-content style=\"fixed-case\">PRR<\/jats:styled-content>\n                    s). The accelerating pace of inflammasome research has demonstrated important roles for inflammasome activation in many pathologic conditions, including infectious, metabolic, autoinflammatory, and autoimmune diseases. The inflammasome generally comprises a\n                    <jats:styled-content style=\"fixed-case\">PRR<\/jats:styled-content>\n                    , procaspase 1, and an adaptor molecule connecting the\n                    <jats:styled-content style=\"fixed-case\">PRR<\/jats:styled-content>\n                    and procaspase 1. Upon inflammasome activation, procaspase 1 becomes active caspase 1 that converts pro\u2013interleukin\u20101\u03b2 (pro\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\u03b2) and pro\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 into mature and active\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\u03b2 and\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018, respectively. The cytokines\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\u03b2 and\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 have multipotent effects on immune and nonimmune cells and induce and promote systemic and local inflammatory responses. Human studies have shown increased levels of these cytokines, altered activation of inflammasome\u2010related molecules, and\/or the presence of inflammasome activators in rheumatic diseases, including systemic lupus erythematosus, rheumatoid arthritis, crystal\u2010induced arthropathies, and Sj\u00f6gren's syndrome. Such changes are found in the primary target organs, such as the kidneys, joints, and salivary glands, as well as in the cardiovascular system. In animal models of rheumatic diseases, inflammation and tissue damage improve upon genetic or pharmacologic targeting of the inflammasome, supporting its pathogenic role. Herein, we review the clinicopathologic significance and therapeutic targeting of inflammasome activation in rheumatic diseases and related conditions based on recent findings.\n                  <\/jats:p>","DOI":"10.1002\/art.41127","type":"journal-article","created":{"date-parts":[[2019,9,28]],"date-time":"2019-09-28T03:10:03Z","timestamp":1569640203000},"page":"386-395","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Advances in Disease Mechanisms and Translational Technologies: Clinicopathologic Significance of Inflammasome Activation in Autoimmune Diseases"],"prefix":"10.1002","volume":"72","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4006-8945","authenticated-orcid":false,"given":"J. 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