{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:13:39Z","timestamp":1786976019605,"version":"build-2736575974"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,8,29]],"date-time":"2025-08-29T00:00:00Z","timestamp":1756425600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FEBS Open Bio"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:p>\n                    Our group has previously reported that inhibin and its molecular pair, TGF\u2010\u03b2 type III receptor (T\u03b2RIII), regulate T\u00a0cell development within the thymus. In addition, inhibins play a key role in immune tolerance through the modulation of dendritic cell (DC) maturation and peripheral Treg induction. However, the functional role of inhibins in T\u00a0cell activation and differentiation is currently unknown. Here, we demonstrate that inhibins are produced by activated T\u00a0cells and play a role during T\u00a0cell activation, migration, and functional Th differentiation. Specifically, stimulation of Inh\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    na\u00efve T\u00a0cells resulted in decreased expression of early activation markers, including CD69, CD25, and T\u03b2RIII, compared to Inh\u03b1\n                    <jats:sup>+\/+<\/jats:sup>\n                    T\u00a0cells. Additionally, we analyzed the migratory potential of Inh\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    T\u00a0cells toward CCR7 ligands and showed an impaired\n                    <jats:italic>in vitro<\/jats:italic>\n                    chemotaxis toward CCL21 and CCL19, which correlated with a decreased homing to peripheral lymph nodes using\n                    <jats:italic>in vivo<\/jats:italic>\n                    competitive assays. To evaluate the impact of inhibins on Th differentiation, we performed\n                    <jats:italic>in vitro<\/jats:italic>\n                    polarization cultures under skewing conditions. Interestingly, Inh\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    na\u00efve T\u00a0cells showed a decreased differentiation to Th1 cells, while the induction of Th17 cells was significantly increased when compared with Inh\u03b1\n                    <jats:sup>+\/+<\/jats:sup>\n                    . This preferential polarization of Inh\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    toward Th17 was reversed by the addition of recombinant Inh A, without altering the differentiation of Inh\u03b1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    Th1. Our data demonstrate that inhibins regulate T\u00a0cell effector differentiation and homing and thus, may be considered new players in T\u00a0cell immune responses.\n                  <\/jats:p>","DOI":"10.1002\/2211-5463.70106","type":"journal-article","created":{"date-parts":[[2025,8,30]],"date-time":"2025-08-30T05:39:27Z","timestamp":1756532367000},"page":"79-89","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Key role for inhibins in effective T\u00a0cell activation, migration and Th17 differentiation"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4275-8253","authenticated-orcid":false,"given":"Sandra","family":"Ortega\u2010Francisco","sequence":"first","affiliation":[{"name":"Departamento de Immunolog\u00eda Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico  Mexico"},{"name":"Laboratorio Nacional de Citometr\u00eda de Flujo 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