{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:26:02Z","timestamp":1790745962416,"version":"4.1.0"},"reference-count":63,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"95","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Immunol."],"published-print":{"date-parts":[[2024,5,3]]},"abstract":"<jats:p>\n                    Understanding the mechanisms that regulate T cell immunity is critical for the development of effective therapies for diseases associated with T cell dysfunction, including autoimmune diseases, chronic infections, and cancer. Co-inhibitory \u201ccheckpoint molecules,\u201d such as programmed cell death protein-1, balance excessive or prolonged immune activation by T cell\u2013intrinsic signaling. Here, by screening for mediators of natural killer (NK) cell recognition on T cells, we identified the immunoglobulin superfamily ligand B7H6 to be highly expressed by activated T cells, including patient-infused CD19-targeting chimeric antigen receptor (CAR) T cells. Unlike other checkpoint molecules, B7H6 mediated NKp30-dependent recognition and subsequent cytolysis of activated T cells by NK cells. B7H6\n                    <jats:sup>+<\/jats:sup>\n                    T cells were prevalent in the tissue and blood of several diseases, and their abundance in tumor tissue positively correlated with clinical response in a cohort of patients with immune checkpoint inhibitor\u2013treated esophageal cancer. In humanized mouse models, NK cell surveillance via B7H6 limited the persistence and antitumor activity of CAR T cells, and its genetic deletion enhanced T cell proliferation and persistence. Together, we provide evidence of B7H6 protein expression by activated T cells and suggest the B7H6-NKp30 axis as a therapeutically actionable NK cell\u2013dependent immune checkpoint that regulates human T cell function.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.adj7970","type":"journal-article","created":{"date-parts":[[2024,5,3]],"date-time":"2024-05-03T13:59:28Z","timestamp":1714744768000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":41,"title":["The immunoglobulin superfamily ligand B7H6 subjects T cell responses to NK cell surveillance"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1946-3174","authenticated-orcid":true,"given":"Michael","family":"Kilian","sequence":"first","affiliation":[{"name":"DKTK Clinical Cooperation Unit (CCU) Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany."},{"name":"Department of Neurology, MCTN, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6401-3623","authenticated-orcid":true,"given":"Mirco J.","family":"Friedrich","sequence":"additional","affiliation":[{"name":"Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA."},{"name":"Department of Hematology, Oncology and Rheumatology, University Hospital Heidelberg, Heidelberg, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5994-3826","authenticated-orcid":true,"given":"Kevin Hai-Ning","family":"Lu","sequence":"additional","affiliation":[{"name":"DKTK Clinical Cooperation Unit (CCU) Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany."},{"name":"Department of Neurology, MCTN, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany."},{"name":"Department of Pediatric 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