{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T18:26:56Z","timestamp":1770229616543,"version":"3.49.0"},"reference-count":48,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T00:00:00Z","timestamp":1770163200000},"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>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Few advances have been made in the treatment of T-cell acute lymphoblastic leukemia (T-ALL). Approaches targeting histone deacetylases (HDAC) have not been thoroughly investigated in T-ALL. However, the underlying molecular mechanism of HDAC inhibition remains to be fully elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>The study aimed to evaluate the clinical outcome of chidamide (an oral selective HDAC inhibitor for HDAC1, HDAC2, HDAC3, and HDAC10) in combination with chemotherapy in relapsed or refractory T-ALL and explore the underlying molecular mechanism of HDAC inhibition in T-ALL.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The clinical outcomes of 28 patients with relapsed or refractory T-ALL, who received chidamide in combination with chemotherapy were first evaluated. Chidamide (30mg per dose) was orally administered twice a week for a total of four doses (120mg in total per patient) during the first 2 weeks of the combined salvage chemotherapy. Transcriptomic analysis was used to identify pivotal signaling pathways of histone deacetylase inhibition in T-ALL cell lines. Short hairpin RNA-mediated inhibition, co-immunoprecipitation, and a series of functional assays were performed to verify the putative signaling pathways involved in cell lines, primary patient samples, and mouse models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Of the 28 patients, 16 achieved a complete response and three achieved a partial response. As an inhibitor of histone deacetylases, chidamide significantly suppressed the proliferation of T-ALL cells and induced apoptosis and cell cycle arrest\n                      <jats:italic>in vitro<\/jats:italic>\n                      . Chidamide treatment significantly inhibited the protein level of HDAC3, but not HDAC1, HDAC2, or HDAC10, in T-ALL cell lines and primary human T-ALL cells. Moreover, the TYK2-STAT1-BCL2 signaling pathway was also substantially inhibited upon chidamide administration. Finally, overexpression of HDAC3 and TYK2 rescued the inhibitory effects of chidamide on T-ALL cells. HDAC3 was found to associate with TYK2 and contributed to activation of the TYK2-STAT1-BCL2 signaling pathway in T-ALL cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our results highlight the effectiveness of the combination of chidamide and chemotherapy in the treatment of T-ALL patients and suggest that HDAC3 can act as a potential novel therapeutic target to inhibit the TYK2-STAT1-BCL2 signaling pathway in T-ALL.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1752727","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T06:44:35Z","timestamp":1770187475000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["HDAC3 inhibition as a therapeutic strategy in T-cell acute lymphoblastic leukemia via the TYK2-STAT1-BCL2 signaling 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