{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T17:28:45Z","timestamp":1790270925657,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,5,22]],"date-time":"2012-05-22T00:00:00Z","timestamp":1337644800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Macrophages altered by various Th2\u2010associated and anti\u2010inflammatory mediators \u2013 including IL\u20104 and IL\u201013 [inducing alternatively activated macrophages (AAMs)], IL\u201010 and TGF\u2010\u03b2\u2013 were generically termed M2. However, markers that discriminate between AAMs and other M2 remain scarce. We previously described E\u2010cadherin as a marker for AAMs, permitting these macrophages to fuse upon IL\u20104 stimulation. To identify novel potential contributors to macrophage fusion, we assessed the effect of IL\u20104 on other adherens and tight junction\u2013associated components. We observed an induction of claudin\u20101 (<jats:italic>Cldn1<\/jats:italic>), <jats:italic>Cldn2<\/jats:italic> and <jats:italic>Cldn11<\/jats:italic> genes by IL\u20104 in different mouse macrophage populations. Extending our findings to other stimuli revealed <jats:italic>Cldn1<\/jats:italic> as a mainly TGF\u2010\u03b2\u2010induced gene and showed that <jats:italic>Cldn11<\/jats:italic> is predominantly associated with IL\u20104\u2010induced AAMs. <jats:italic>Cldn2<\/jats:italic> is upregulated by diverse stimuli and is not associated with a specific macrophage activation state <jats:italic>in vitro<\/jats:italic>. Interestingly, different claudin genes preferentially associate with M2 from distinct diseases. While <jats:italic>Cldn11<\/jats:italic> is predominantly expressed in AAMs from helminth\u2010infected mice, <jats:italic>Cldn1<\/jats:italic> is the major macrophage claudin during chronic trypanosomiasis and <jats:italic>Cldn2<\/jats:italic> dominates in tumour\u2010associated macrophages. Overall, we identified <jats:italic>Cldn1<\/jats:italic>, <jats:italic>Cldn2<\/jats:italic> and <jats:italic>Cldn11<\/jats:italic> as genes that discriminate between diverse types of M2.<\/jats:p>","DOI":"10.1111\/j.1365-3083.2012.02689.x","type":"journal-article","created":{"date-parts":[[2012,1,23]],"date-time":"2012-01-23T12:55:42Z","timestamp":1327323342000},"page":"588-598","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Claudin\u20101, Claudin\u20102 and Claudin\u201011 Genes Differentially Associate with Distinct Types of Anti\u2010inflammatory Macrophages <i>In vitro<\/i> and with Parasite\u2010 and Tumour\u2010elicited Macrophages <i>In vivo<\/i>"],"prefix":"10.1111","volume":"75","author":[{"given":"J.","family":"Van den Bossche","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Laoui","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Morias","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Movahedi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G.","family":"Raes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"De Baetselier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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