{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T04:05:14Z","timestamp":1790309114524,"version":"4.1.0"},"reference-count":38,"publisher":"Rockefeller University Press","issue":"6","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1999,3,15]]},"abstract":"<jats:p>For T cells to become functionally activated they require at least two signals. The B7 costimulatory molecules B7-1 and B7-2 provide the \u201csecond signal\u201d pivotal for T cell activation. In this report, we studied the relative roles of B7-1 and B7-2 molecules in the induction of antitumor immunity to the T cell thymoma, EL4. We generated EL4 tumor cells that expressed B7-1, B7-2, and B7-1+B7-2 by transfecting murine cDNAs. Our results demonstrate that EL4\u2013B7-1 cells are completely rejected in syngeneic mice. Unlike EL4\u2013B7-1 cells, we find that EL4\u2013B7-2 cells are not rejected but progressively grow in the mice. A B7-1\u2013 and B7-2\u2013EL4 double transfectant was generated by introducing B7-2 cDNA into the EL4\u2013B7-1 tumor line that regressed in vivo. The EL4\u2013B7-1+B7-2 double transfectant was not rejected when implanted into syngeneic mice but progressively grew to produce tumors. The double transfectant EL4 cells could costimulate T cell proliferation that could be blocked by anti\u2013B7-1 antibodies, anti\u2013B7-2 antibodies, or hCTLA4 immunoglobulin, showing that the B7-1 and B7-2 molecules expressed on the EL4 cells were functional. In vivo, treatment of mice implanted with double-transfected EL4 cells with anti\u2013B7-2 monoclonal antibody resulted in tumor rejection. Furthermore, the EL4\u2013B7-2 and EL4\u2013B7-1+B7-2 cells, but not the wild-type EL4 cells, were rejected in interleukin 4 (IL-4) knockout mice. Our data suggests that B7-2 expressed on some T cell tumors inhibits development of antitumor immunity, and IL-4 appears to play a critical role in abrogation of the antitumor immune response.<\/jats:p>","DOI":"10.1084\/jem.189.6.919","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:48:33Z","timestamp":1027702113000},"page":"919-930","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":39,"title":["B7-2 Expressed on EL4 Lymphoma Suppresses Antitumor Immunity by an Interleukin 4\u2013dependent Mechanism"],"prefix":"10.1084","volume":"189","author":[{"given":"C.","family":"Stremmel","sequence":"first","affiliation":[{"name":"From the *Center for Neurological Diseases, Brigham and Women's Hospital, and Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115; and the \u2021Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.A.","family":"Greenfield","sequence":"additional","affiliation":[{"name":"From the *Center for Neurological Diseases, Brigham and Women's Hospital, and Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115; and the \u2021Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115"},{"name":"From the *Center for Neurological Diseases, Brigham and Women's Hospital, and Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115; and the \u2021Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Howard","sequence":"additional","affiliation":[{"name":"From the *Center for Neurological Diseases, Brigham and Women's Hospital, and Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115; and the \u2021Department of Adult 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