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Gene-targeted mice have recently revealed a role for lymphocytes and interferon- gamma (IFN gamma ) in conferring protection against cancer, but the mechanisms remain unclear. Here, we have characterized a successful primary antitumor immune response initiated by naive CD4 super(+) T cells. Major histocompatibility complex class II (MHC-II)-negative myeloma cells injected subcutaneously into syngeneic mice were surrounded within 3 days by macrophages that captured tumor antigens. Within 6 days, naive myeloma-specific CD4 super(+) T cells became activated in draining lymph nodes and subsequently migrated to the incipient tumor site. Upon recognition of tumor-derived antigenic peptides presented on MHC-II by macrophages, the myeloma-specific CD4 super(+) T cells were reactivated and started to secrete cytokines. T cell-derived IFN gamma activated macrophages in close proximity to the tumor cells. Tumor cell growth was completely inhibited by such locally activated macrophages. These data indicate a mechanism for immunosurveillance of MHC-II-negative cancer cells by tumor-specific CD4 super(+) T cells through collaboration with macrophages.
Sprache
Englisch
Identifikatoren
ISSN: 1074-7613
eISSN: 1097-4180
DOI: 10.1016/j.immuni.2005.02.003
Titel-ID: cdi_proquest_miscellaneous_17856132
Format
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