{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T14:32:07Z","timestamp":1785335527070,"version":"3.55.0"},"reference-count":69,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,1,29]],"date-time":"2024-01-29T00:00:00Z","timestamp":1706486400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Interleukin (IL)-17-producing \u03b3\u03b4T (\u03b3\u03b4T17) cells mediate inflammatory responses in barrier tissues. Dysregulated \u03b3\u03b4T17 cell activation can lead to the overproduction of IL-17 and IL-22 and the development of inflammatory diseases, including psoriasis. IL-23 and IL-1\u03b2 are known to synergistically activate \u03b3\u03b4T17 cells, but the regulatory mechanisms of \u03b3\u03b4T17 cells have not been fully elucidated. This study aimed to reveal the contribution of the inflammatory cytokine tumor necrosis factor-like ligand 1A (TL1A) to \u03b3\u03b4T17 cell activation and psoriasis development.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Anti-TL1A antibody was injected into an imiquimod (IMQ)-induced murine psoriasis model. TL1A receptor expression was analyzed in splenic and dermal \u03b3\u03b4T cells. \u03b3\u03b4T cells were tested for cytokine production <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> under stimulation with IL-23, IL-1\u03b2, and TL1A. TL1A was applied to a psoriasis model induced by intradermal IL-23 injection. Mice deficient in \u03b3\u03b4T cells were intradermally injected with IL-23 plus TL1A to verify the contribution of TL1A-dependent \u03b3\u03b4T-cell activation to psoriasis development.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Neutralization of TL1A attenuated \u03b3\u03b4T17 cell activation in IMQ-treated skin. TL1A induced cytokine production by splenic \u03b3\u03b4T17 cells in synergy with IL-23. Dermal \u03b3\u03b4T17 cells constitutively expressed a TL1A receptor at high levels and vigorously produced IL-22 upon intradermal IL-23 and TL1A injection but not IL-23 alone. TL1A exacerbated the dermal symptoms induced by IL-23 injection in wild-type but not in \u03b3\u03b4T cell\u2013deficient mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings suggest a novel regulatory mechanism of \u03b3\u03b4T cells through TL1A and its involvement in psoriasis pathogenesis as a possible therapeutic target.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fimmu.2024.1340467","type":"journal-article","created":{"date-parts":[[2024,1,29]],"date-time":"2024-01-29T04:33:05Z","timestamp":1706502785000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Roles of tumor necrosis factor-like ligand 1A in \u03b3\u03b4T-cell activation and psoriasis pathogenesis"],"prefix":"10.3389","volume":"15","author":[{"given":"Shangyi","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mina","family":"Kozai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaya","family":"Hiraishi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Md. 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