title: Claudin-1, claudin-2 and claudin-11 genes differentially associate with distinct types of anti-inflammatory macrophages in vitro and with parasite- and tumour-elicited macrophages in vivo.
abstract: Macrophages altered by various Th2-associated and anti-inflammatory mediators--including IL-4 and IL-13 [inducing alternatively activated macrophages (AAMs)], IL-10 and TGF-β--were generically termed M2. However, markers that discriminate between AAMs and other M2 remain scarce. We previously described E-cadherin as a marker for AAMs, permitting these macrophages to fuse upon IL-4 stimulation. To identify novel potential contributors to macrophage fusion, we assessed the effect of IL-4 on other adherens and tight junction-associated components. We observed an induction of claudin-1 (Cldn1), Cldn2 and Cldn11 genes by IL-4 in different mouse macrophage populations. Extending our findings to other stimuli revealed Cldn1 as a mainly TGF-β-induced gene and showed that Cldn11 is predominantly associated with IL-4-induced AAMs. Cldn2 is upregulated by diverse stimuli and is not associated with a specific macrophage activation state in vitro. Interestingly, different claudin genes preferentially associate with M2 from distinct diseases. While Cldn11 is predominantly expressed in AAMs from helminth-infected mice, Cldn1 is the major macrophage claudin during chronic trypanosomiasis and Cldn2 dominates in tumour-associated macrophages. Overall, we identified Cldn1, Cldn2 and Cldn11 as genes that discriminate between diverse types of M2.
authors.affiliation: Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium             Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
authors.forename: J
authors.initials: J
authors.lastname: Van den Bossche
authors.forename: D
authors.initials: D
authors.lastname: Laoui
authors.forename: Y
authors.initials: Y
authors.lastname: Morias
authors.forename: K
authors.initials: K
authors.lastname: Movahedi
authors.forename: G
authors.initials: G
authors.lastname: Raes
authors.forename: P
authors.initials: P
authors.lastname: De Baetselier
authors.forename: J A
authors.initials: JA
authors.lastname: Van Ginderachter
mesh_terms: D000230:Adenocarcinoma / Q000276:immunology; D000818:Animals; D015153:Blotting, Western; D002469:Cell Separation; D062445:Claudin-1; D057167:Claudins / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D007249:Inflammation / Q000276:immunology*; D015847:Interleukin-4 / Q000276:immunology; D008262:Macrophage Activation / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D008565:Membrane Proteins / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009419:Nerve Tissue Proteins / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013622:Taeniasis / Q000276:immunology; D014352:Trypanosomiasis / Q000276:immunology
chemical_list: D062445:Claudin-1; D057167:Claudins; C568113:Cldn1 protein, mouse; C492354:Cldn11 protein, mouse; C113371:Cldn2 protein, mouse; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D015847:Interleukin-4