{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T10:48:40Z","timestamp":1770720520521,"version":"3.49.0"},"reference-count":46,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2005,11,17]],"date-time":"2005-11-17T00:00:00Z","timestamp":1132185600000},"content-version":"vor","delay-in-days":3853,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1995,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Although the transfection of B7\u20101 cDNA into a few mouse tumor cell lines can induce anti\u2010tumor T cell immunity, its expression alone is ineffective in many other tumor cell lines tested. We were interested to study what factors limit B7\u20101 co\u2010stimulatory activity, and decided to investigate whether B7\u20101 requires the cooperation of ICAM\u20101 to provide the minimal co\u2010stimulatory signal for establishing an efficient anti\u2010tumor immunity. We show that the transfection of B7\u20101 cDNA into three ICAM\u20101<jats:sup>+<\/jats:sup> (plasmocytoma J558L, T lymphomas EL\u20104 and RMA), but not into two ICAM\u20101<jats:sup>\u2212<\/jats:sup> tumor cell lines (adenocarcinoma TS\/A and melanoma B16.F1), is sufficient to induce their complete rejection in syngeneic mice. The expression of ICAM\u20101 is necessary for the rejection of the B7 expressing tumors, since the primary response elicited by B7\u20101<jats:sup>+<\/jats:sup> EL\u20104 and RMA clones expressing reduced levels of ICAM\u20101 is severely reduced. Furthermore, super\u2010transfection of ICAM\u20101 cDNA into B7\u20101<jats:sup>+<\/jats:sup> adenocarcinoma and melanoma clones optimizes their primary rejection. Histologic examination of transfected tumors reveals that B7\u20101 and ICAM\u20101 exert a potent pro\u2010inflammatory activity. The intra\u2010tumor infiltration is composed of both eosinophils and lymphomono\u2010cytes, and is already massive 5 days after the tumor challenge. The primary rejection of the B7\u20101<jats:sup>+<\/jats:sup> ICAM\u20101<jats:sup>+<\/jats:sup> tumors depends critically on CD8<jats:sup>+<\/jats:sup> T cells, natural killer cells and granulocytes, but is independent of CD4<jats:sup>+<\/jats:sup> T cells. Remarkably, in addition to its effects on the early phases of the immune response, the co\u2010expression of ICAM\u20101 and B7\u20101 on tumors is also necessary for the efficient induction of a memory response. In fact, only the primary challenge with B7\u20101<jats:sup>+<\/jats:sup>, ICAM\u20101<jats:sup>+<\/jats:sup> tumor cells protects the majority of the mice from a second injection of parental tumor cells. Collectively, our findings indicate that B7\u20101 and ICAM\u20101 are fundamental components for triggering the primary rejection of tumors and establishing a protective memory response. These findings may help to define new strategies for the rational application of co\u2010stimulation in tumor immunotherapy.<\/jats:p>","DOI":"10.1002\/eji.1830250504","type":"journal-article","created":{"date-parts":[[2007,3,2]],"date-time":"2007-03-02T01:07:04Z","timestamp":1172797624000},"page":"1154-1162","source":"Crossref","is-referenced-by-count":82,"title":["Co\u2010expression of B7\u20101 and ICAM\u20101 on tumors is required for rejection and the establishment of a memory response"],"prefix":"10.1002","volume":"25","author":[{"given":"Federica","family":"Cavallo","sequence":"first","affiliation":[]},{"given":"Alfonso","family":"Martin\u2010Fontecha","sequence":"additional","affiliation":[]},{"given":"Matteo","family":"Bellone","sequence":"additional","affiliation":[]},{"given":"Silvia","family":"Heltai","sequence":"additional","affiliation":[]},{"given":"Evelina","family":"Gatti","sequence":"additional","affiliation":[]},{"given":"Paola","family":"Tornaghi","sequence":"additional","affiliation":[]},{"given":"Massimo","family":"Freschi","sequence":"additional","affiliation":[]},{"given":"Guido","family":"Forni","sequence":"additional","affiliation":[]},{"given":"Paolo","family":"Dellabona","sequence":"additional","affiliation":[]},{"given":"Giulia","family":"Casorati","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2005,11,17]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90844-1"},{"key":"e_1_2_1_3_2","first-page":"35","volume-title":"The Biologic Therapy of Cancer","author":"Hellstr\u00f6m K. 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