{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T22:35:17Z","timestamp":1788388517294,"version":"build-2803163510"},"reference-count":81,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,9,10]],"date-time":"2013-09-10T00:00:00Z","timestamp":1378771200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Lichen planopilaris (\n                    <jats:styled-content style=\"fixed-case\">LPP<\/jats:styled-content>\n                    ) is a chronic inflammatory disease of unknown pathogenesis that leads to permanent hair loss. Whilst destruction of epithelial hair follicle stem cells (\n                    <jats:styled-content style=\"fixed-case\">eHFSCs<\/jats:styled-content>\n                    ) that reside in an immunologically protected niche of the\n                    <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n                    epithelium, the bulge, is a likely key event in\n                    <jats:styled-content style=\"fixed-case\">LPP<\/jats:styled-content>\n                    pathogenesis, this remains to be demonstrated. We have tested the hypotheses that bulge immune privilege (\n                    <jats:styled-content style=\"fixed-case\">IP<\/jats:styled-content>\n                    ) collapse and inflammation\u2010induced\n                    <jats:styled-content style=\"fixed-case\">eHFSC<\/jats:styled-content>\n                    death are key components in the pathogenesis of\n                    <jats:styled-content style=\"fixed-case\">LPP<\/jats:styled-content>\n                    . Biopsies of lesional and non\u2010lesional scalp skin from adult\n                    <jats:styled-content style=\"fixed-case\">LPP<\/jats:styled-content>\n                    patients (\n                    <jats:italic>n =<\/jats:italic>\n                    42) were analysed by quantitative (immuno)histomorphometry, real\u2010time quantitative polymerase chain reaction (\n                    <jats:styled-content style=\"fixed-case\">qRT\u2013PCR<\/jats:styled-content>\n                    ), laser capture microdissection and microarray analysis, or skin organ culture. At both the protein and transcriptional level, lesional\n                    <jats:styled-content style=\"fixed-case\">LPP HFs<\/jats:styled-content>\n                    showed evidence for bulge\n                    <jats:styled-content style=\"fixed-case\">IP<\/jats:styled-content>\n                    collapse (ie increased expression of\n                    <jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content>\n                    class I and\n                    <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                    ,\n                    <jats:italic>\u03b2<\/jats:italic>\n                    2microglobulin; reduced TGF\n                    <jats:italic>\u03b2<\/jats:italic>\n                    2 and CD200 expression). This was accompanied by a Th1\u2010biased cytotoxic T cell response (ie increased CD8\n                    <jats:sup>+<\/jats:sup>\n                    GranzymeB\n                    <jats:sup>+<\/jats:sup>\n                    T cells and CD123\n                    <jats:sup>+<\/jats:sup>\n                    plasmacytoid dendritic cells, with increased CXCR3 expression) and increased expression of interferon\u2010inducible chemokines (CXCL9\/10\/11). Interestingly, lesional LPP eHFSCs showed both increased proliferation and apoptosis\n                    <jats:italic>in situ<\/jats:italic>\n                    . Microarray analysis revealed a loss of eHFSC signatures and increased expression of T cell activation\/binding markers in active LPP, while bulge PPAR\n                    <jats:italic>\u03b3<\/jats:italic>\n                    transcription was unaltered compared to non\u2010lesional LPP HFs. In organ culture of non\u2010lesional LPP skin, interferon\u2010\n                    <jats:italic>\u03b3<\/jats:italic>\n                    (IFN\n                    <jats:italic>\u03b3<\/jats:italic>\n                    ) induced bulge IP collapse. LPP is an excellent model disease for studying and preventing immune destruction of human epithelial stem cells\n                    <jats:italic>in situ<\/jats:italic>\n                    . These novel findings raise the possibility that LPP represents an autoimmune disease in whose pathogenesis IFN\n                    <jats:italic>\u03b3<\/jats:italic>\n                    \u2010induced bulge IP collapse plays an important role. Therapeutically, bulge IP protection\/restoration may help to better manage this highly treatment\u2010resistant cicatricial alopecia. Copyright \u00a9 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.4233","type":"journal-article","created":{"date-parts":[[2013,6,20]],"date-time":"2013-06-20T14:26:39Z","timestamp":1371738399000},"page":"236-247","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":244,"title":["Lichen planopilaris is characterized by immune privilege collapse of the hair follicle's epithelial stem cell niche"],"prefix":"10.1002","volume":"231","author":[{"given":"Matthew J","family":"Harries","sequence":"first","affiliation":[{"name":"Dermatology Centre, Salford Royal NHS Foundation Trust, University of Manchester Manchester Academic Health Science Centre UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katja","family":"Meyer","sequence":"additional","affiliation":[{"name":"Department of Dermatology University of L\u00fcbeck 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