{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T05:10:12Z","timestamp":1790917812272,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2011,5,16]],"date-time":"2011-05-16T00:00:00Z","timestamp":1305504000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2011,9]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> Keratinocytes synthesize complement component 3 (C3) constitutively, and increased expression of C3 has been described during skin inflammation. In this study, we investigated the role of C3 in T cell\u2010mediated allergic contact dermatitis, which is a clinical manifestation of contact sensitivity (CS). C3\u2010deficient mice (C3KO) showed substantial higher CS responses to haptens, inducing a Th1 cytokine\u2010mediated skin inflammation (2,4\u2010dinitrofluorobenzene and dinitrochlorobenzene), and to haptens known to induce a Th2\u2010polarized inflammatory response (fluoro\u2010isothiocynate and toluene\u20102,4\u2010diisocyanate) as compared to their wild\u2010type (WT) controls. There was a higher influx of GR\u20101<jats:sup>+<\/jats:sup>, CD4<jats:sup>+<\/jats:sup>, and CD8<jats:sup>+<\/jats:sup> cells into the skin of hapten\u2010treated C3KO mice compared with WT mice. Activated splenocytes from C3KO mice immunized with DNCB secreted higher amounts of IFN\u2010\u03b3 compared with WT controls but not of Th2 (IL\u20104, IL\u20105, and IL\u201010) cytokines or IL\u201017. A higher secretion of IL\u201012 from splenocytes of C3KO mice as compared with WT mice was observed after TLR\u20104 ligand (LPS) or TLR\u20102 ligand (peptidoglycan) stimulation. Thus, an increased expression of IL\u201012 and of IFN\u2010\u03b3 may be responsible for the increased hapten\u2010induced inflammation in C3 deficiency. Finally, we demonstrated that C3KO mice developed oral tolerance to haptens to a lower degree than WT mice. Our findings provide a new insight into a novel anti\u2010inflammatory role of C3 in skin inflammation.<\/jats:p>","DOI":"10.1111\/j.1600-0625.2011.01295.x","type":"journal-article","created":{"date-parts":[[2011,5,16]],"date-time":"2011-05-16T08:32:30Z","timestamp":1305534750000},"page":"709-714","source":"Crossref","is-referenced-by-count":19,"title":["A protective role of complement component 3 in T cell\u2010mediated skin 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