{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,6]],"date-time":"2025-11-06T16:04:47Z","timestamp":1762445087824,"version":"3.40.5"},"reference-count":71,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,11,4]],"date-time":"2020-11-04T00:00:00Z","timestamp":1604448000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2021,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Fatty acid\u2010binding protein 3 (FABP3) is a cytosolic carrier protein of polyunsaturated fatty acids (PUFAs) and regulates cellular metabolism. However, the physiological functions of FABP3 in immune cells and how FABP3 regulates inflammatory responses remain unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Contact hypersensitivity (CHS) induced by 2,4\u2010dinitrofluorobenzene (DNFB) and fluorescein isothiocyanate was applied to the skin wild\u2010type and <jats:italic>Fabp3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice. Skin inflammation was assessed using FACS, histological, and qPCR analyses. The development of \u03b3\/\u03b4 T cells was evaluated by a co\u2010culture system with OP9\/Dll1 cells in the presence or absence of transgene of FABP3.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Fabp3\u2010deficient mice exhibit a more severe phenotype of contact hypersensitivity (CHS) accompanied by infiltration of IL\u201017\u2010producing V\u03b34<jats:sup>+<\/jats:sup> \u03b3\/\u03b4 T cells that critically control skin inflammation. In <jats:italic>Fabp3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice, we found a larger proportion of V\u03b34<jats:sup>+<\/jats:sup> \u03b3\/\u03b4 T cells in the skin, even though the percentage of total \u03b3\/\u03b4 T cells did not change at steady state. Similarly, juvenile <jats:italic>Fabp3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice also contained a higher amount of V\u03b34<jats:sup>+<\/jats:sup> \u03b3\/\u03b4 T cells not only in the skin but in the thymus when compared with wild\u2010type mice. Furthermore, thymic double\u2010negative (DN) cells expressed FABP3, and FABP3 negatively regulates the development of V\u03b34<jats:sup>+<\/jats:sup> \u03b3\/\u03b4 T cells in the thymus.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings suggest that FABP3 functions as a negative regulator of skin inflammation through limiting pathogenic V\u03b34<jats:sup>+<\/jats:sup> \u03b3\/\u03b4 T\u2010cell generation in the thymus.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.14630","type":"journal-article","created":{"date-parts":[[2020,10,22]],"date-time":"2020-10-22T17:01:32Z","timestamp":1603386092000},"page":"1776-1788","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Fatty acid\u2010binding protein 3 controls contact hypersensitivity through regulating skin dermal V\u03b34<sup>+<\/sup> \u03b3\/\u03b4 T cell in a murine 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