{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T02:08:15Z","timestamp":1792548495687,"version":"4.5.0"},"reference-count":29,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2006,8,30]],"date-time":"2006-08-30T00:00:00Z","timestamp":1156896000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cutan Pathol"],"published-print":{"date-parts":[[2006,10]]},"abstract":"<jats:p><jats:bold>Introduction:\u2002<\/jats:bold> Lichen planus (LP) is an inflammatory autoimmune skin disease of unknown origin. Evidence has accumulated that autoreactive cytotoxic CD8<jats:sup>+<\/jats:sup> T lymphocytes cause destruction of keratinocytes. Recent studies suggested that type I interferons (IFNs) play a central role in cytotoxic skin inflammation by increasing the expression of IP10\/CXCR10 and recruiting effector cells via CXCR3. Here, we investigated whether type I IFNs are also involved in the pathogenesis of LP.<\/jats:p><jats:p><jats:bold>Patients and methods:\u2002<\/jats:bold> Skin biopsies of altogether 17 donors (seven LP and 10 healthy controls) were analyzed by immunohistochemistry using monoclonal antibodies against CD3, CD4, CD8, CD20, CD68, CXCR3, granzyme B, IP10\/CXCL10, CD123, and the MxA protein, which is specifically induced by type I IFNs.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Our analysis revealed a significant expression of the MxA protein in all LP skin biopsies, indicating involvement of type I IFNs. Expression of MxA was closely associated with the recruitment of CXCR3<jats:sup>+<\/jats:sup> and granzyme B<jats:sup>+<\/jats:sup> lymphocytes, indicating a Th1\u2010biased cytotoxic immune response. Strong expression of the CXCR3 ligand, the interferon\u2010inducible protein IP10\/CXCL10, links type I IFN expression and recruitment of CXCR3<jats:sup>+<\/jats:sup> lymphocytes. Plasmacytoid dendritic cells (pDCs) appear to be a major source of type I IFNs in LP.<\/jats:p><jats:p><jats:bold>Discussion:\u2002<\/jats:bold> Our observations support the hypothesis that lesional type I IFNs produced by pDCs plays an important role in chronic cytotoxic inflammation of LP by recruiting cytotoxic effector lymphocytes via IP10\/CXCR3 interactions.<\/jats:p>","DOI":"10.1111\/j.1600-0560.2006.00527.x","type":"journal-article","created":{"date-parts":[[2006,8,30]],"date-time":"2006-08-30T19:43:32Z","timestamp":1156967012000},"page":"672-678","source":"Crossref","is-referenced-by-count":109,"title":["Type I interferon\u2010associated cytotoxic inflammation in lichen 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