{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T22:11:16Z","timestamp":1790374276547,"version":"4.1.0"},"reference-count":101,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2018,1,31]],"date-time":"2018-01-31T00:00:00Z","timestamp":1517356800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Histochem Cytochem."],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:p>To protect against danger, the innate immune system must promptly and accurately sense alarm signals, and mount an appropriate response to restore homeostasis. One endogenous trigger of immunity is tenascin-C, a large hexameric protein of the extracellular matrix. Upregulated upon tissue injury and cellular stress, tenascin-C is expressed during inflammation and tissue remodeling, where it influences cellular behavior by interacting with a multitude of molecular targets, including other matrix components, cell surface proteins, and growth factors. Here, we discuss how these interactions confer upon tenascin-C distinct immunomodulatory capabilities that make this matrix molecule necessary for efficient tissue repair. We also highlight in vivo studies that provide insight into the consequences of misregulated tenascin-C expression on inflammation and fibrosis during a wide range of inflammatory diseases. Finally, we examine how its unique expression pattern and inflammatory actions make tenascin-C a viable target for clinical exploitation in both diagnostic and therapeutic arenas.<\/jats:p>","DOI":"10.1369\/0022155418757443","type":"journal-article","created":{"date-parts":[[2018,1,31]],"date-time":"2018-01-31T19:00:03Z","timestamp":1517425203000},"page":"289-304","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":90,"title":["Internal Affairs: Tenascin-C as a Clinically Relevant, Endogenous Driver of Innate Immunity"],"prefix":"10.1369","volume":"66","author":[{"given":"Anna M.","family":"Marzeda","sequence":"first","affiliation":[{"name":"Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kim 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