{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T16:14:55Z","timestamp":1784823295952,"version":"3.55.0"},"reference-count":53,"publisher":"BMJ","issue":"4","license":[{"start":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T00:00:00Z","timestamp":1775088000000},"content-version":"unspecified","delay-in-days":1,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003407","name":"Ministero dell\u2019Istruzione, dell\u2019Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["Project PE_00000019"],"award-info":[{"award-number":["Project PE_00000019"]}],"id":[{"id":"10.13039\/501100003407","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007366","name":"Fondazione Italiana Sclerosi Multipla","doi-asserted-by":"publisher","award":["2019\/RVsingle\/053"],"award-info":[{"award-number":["2019\/RVsingle\/053"]}],"id":[{"id":"10.13039\/100007366","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005010","name":"Associazione Italiana per la Ricerca sul Cancro","doi-asserted-by":"publisher","award":["IGV19939"],"award-info":[{"award-number":["IGV19939"]}],"id":[{"id":"10.13039\/501100005010","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002915","name":"Fondation pour la Recherche M\u00e9dicale","doi-asserted-by":"publisher","award":["RAD21006CCA INSERM TRANSFERT R19073CS"],"award-info":[{"award-number":["RAD21006CCA INSERM TRANSFERT R19073CS"]}],"id":[{"id":"10.13039\/501100002915","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000289","name":"Cancer Research UK","doi-asserted-by":"publisher","award":["A26813"],"award-info":[{"award-number":["A26813"]}],"id":[{"id":"10.13039\/501100000289","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000289","name":"Cancer Research UK","doi-asserted-by":"publisher","award":["Project 620 Id.!22794"],"award-info":[{"award-number":["Project 620 Id.!22794"]}],"id":[{"id":"10.13039\/501100000289","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2026,1,19]]},"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>We investigated the hypothesis that transforming growth factor \u03b2 induced (TGFBI), an extracellular matrix protein secreted in the microenvironment of several tumors, can act as a secreted immune checkpoint (sIC) that contributes to the suppression of human antitumor T cell responses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>\n                      Serum TGFBI concentrations, measured by ELISA, were significantly higher in patients with colorectal cancer (CRC) and hepatocellular carcinoma than in healthy individuals and associated with poor overall survival. Strikingly, multiparametric flow cytometry analyses revealed that TGFBI was abundantly expressed by tumor cells or monocytes, and by various lymphoid cell types\u2014including CD4\n                      <jats:sup>+<\/jats:sup>\n                      or CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells (including tissue-resident memory T cells), B cells, and natural killer cells\u2014in patients with cancer. Importantly, ex vivo TGFBI neutralization significantly enhanced CD4\n                      <jats:sup>+<\/jats:sup>\n                      and CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell activation and function. Freshly isolated TGFBI-expressing CD4\n                      <jats:sup>+<\/jats:sup>\n                      or CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells demonstrated a markedly improved capacity to differentiate into functional effector cells\u2014characterized by the acquisition of tissue-homing phenotypes\u2014following TGFBI blockade. These findings suggest that TGFBI can establish an autocrine immunosuppressive loop within T cells, thereby limiting their differentiation and function. These mechanistic observations were further supported by human CRC organoid-based experiments, where TGFBI blockade improved expansion and tumor cell killing by major histocompatibility complex class I-restricted cytotoxic T cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Taken together, our data demonstrate that TGFBI acts as a sIC counter-regulating T cell activation, differentiation, and effector function, which can be restored by TGFBI blockade, with broad implications for novel immunotherapy strategies in solid tumors.<\/jats:p>\n                  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