Contributors: Unité différenciation épidermique et auto-immunité rhumatoïde (UDEAR); Université Toulouse III - Paul Sabatier (UT3); Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM); Université de Liège; Walloon Excellence in Life sciences and BIOtechnology Liège (WELBIO); Department of Pathology Stanford; Stanford Medicine; Stanford University-Stanford University; Department of Microbiology and Immunology Stanford; Sean N. Parker Center for Allergy and Asthma Research Stanford; Anticorps en thérapie et pathologie - Antibodies in Therapy and Pathology; Institut Pasteur Paris (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM); NG was supported by the French “Fondation pour la Recherche Médicale FRM” award number SPE20130326582, the Société Française de Dermatologie (SFD), the Société Française l’Allergologie (SFA), the European Commission (Marie Skłodowska-Curie Individual Fellowship H2020-MSCA-IF-2016 749629), and the French “Institut National de la Santé et de la Recherche Médicale” (INSERM); TM is a Research Associate of the F.R.S.-FNRS and is supported by an “Incentive Grant for Scientific Research” of the F.R.S.-FNRS (F.4508.18), by the FRFS-WELBIO under grant CR-2017s-04 and by the Acteria Foundation; SJG is supported by NIH Grants U19 AI104209, R01 AR067145, and R01 AI32494; the United States-Israel Binational Science Foundation (Grant 2013263); the University of California, Tobacco-Related Disease Research Program; and the Sean N. Parker Center for Allergy and Asthma Research, Stanford University; LLR acknowledges support from the European Commission (Marie Skłodowska-Curie Individual Fellowship H2020-MSCA-IF-2014 656086) and the INSERM.; European Project: 749629,H2020-EU.1.3.2. - Nurturing excellence by means of cross-border and cross-sector mobility ,H2020-MSCA-IF-2016,NEMESIS(2017); European Project: 656086,H2020,H2020-MSCA-IF-2014,AllergyBLOCK(2015)
نبذة مختصرة : International audience ; Contact hypersensitivity (CHS) is a common T cell-mediated skin disease induced by epicutaneous sensitization to haptens. Mast cells (MCs) are widely deployed in the skin and can be activated during CHS responses to secrete diverse products, including some with pro-inflammatory and anti-inflammatory functions. Conflicting results have been obtained regarding pathogenic versus protective roles of MCs in CHS, and this has been attributed in part to the limitations of certain models for studying MC functions in vivo. This review discusses recent advances in the development and analysis of mouse models to investigate the roles of MCs and MC-associated products in vivo. Notably, fluorescent avidin-based two-photon imaging approaches enable in vivo selective labeling and simultaneous tracking of MC secretory granules (e.g., during MC degranulation) and MC gene activation by real-time longitudinal intravital microscopy in living mice. The combination of such genetic and imaging tools has shed new light on the controversial role played by MCs in mouse models of CHS. On the one hand, they can amplify CHS responses of mild severity while, on the other hand, can limit the inflammation and tissue injury associated with more severe or chronic models, in part by representing an initial source of the anti-inflammatory cytokine IL-10.
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