{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T06:35:14Z","timestamp":1771482914975,"version":"3.50.1"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2005,8,1]],"date-time":"2005-08-01T00:00:00Z","timestamp":1122854400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Many tumor Ags recognized by T cells are self-Ags. Because high avidity, self-reactive T cells are deleted in the thymus, any residual self-reactive T cells existing in the periphery are likely to be low avidity and nonresponsive due to peripheral tolerance mechanisms. Activation of these residual T cells is critical for targeting tumors for immunotherapy. In this study, we studied immune responses against the murine B16 melanoma using a tyrosinase-related protein 2 (TRP-2) peptide as a model tumor\/self-Ag. Our results showed that TRP-2 peptide vaccination alone elicited a weak T cell response and modestly decreased B16 lung tumor nodules. The combination of peptide vaccination and treatment with an Ab directed against the inhibitory receptor CTLA-4 enhanced the immune response against TRP-2 peptide, inducing autoimmune depigmentation and further decreasing lung tumor nodules. However, both vaccination methods failed to protect against orthotopic (s.c.) B16 tumor challenge. The addition of an irradiated GM-CSF-expressing, amelanotic tumor cell vaccine significantly delayed s.c. B16 tumor growth. Subsequent studies revealed that provision of GM-CSF increased dendritic cell numbers in lymph nodes and spleen. Furthermore, addition of CTLA-4 blockade increased the frequency of TRP-2-specific, IFN-secreting T cells in spleen and lymph nodes. Overall, our results indicate that combining enhancement of Ag presentation with removal of CTLA-4-mediated inhibition can convert a \u201cweaker\u201d autoimmune response into a more potent antitumor immune response.<\/jats:p>","DOI":"10.4049\/jimmunol.175.3.1456","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T23:20:32Z","timestamp":1398036032000},"page":"1456-1463","source":"Crossref","is-referenced-by-count":25,"title":["Provision of Granulocyte-Macrophage Colony-Stimulating Factor Converts an Autoimmune Response to a Self-Antigen into an Antitumor Response"],"prefix":"10.1093","volume":"175","author":[{"given":"Qingyong","family":"Ji","sequence":"first","affiliation":[{"name":"Tumor Immunity and Tolerance Section, Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick Cancer Research and Development Center , Frederick, MD 21702"},{"name":"Department of Microbiology and Immunology, State University of New York, Upstate Medical University , Syracuse, NY 13210"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Gondek","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, State University of New York, Upstate Medical University , Syracuse, NY 13210"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arthur A","family":"Hurwitz","sequence":"additional","affiliation":[{"name":"Tumor Immunity and Tolerance Section, Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick Cancer Research and Development Center , Frederick, MD 21702"},{"name":"Department of Microbiology and Immunology, State University of New York, Upstate Medical University , Syracuse, NY 13210"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,8,1]]},"reference":[{"key":"2026020214054419800_R1","first-page":"85","volume-title":"Immunol. 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