Efficient T cell activation requires two synergistic but distinct signals derived from antigenic peptides presented by the MHC and from costimulatory molecules, particularly those belonging to the B7 family. Lack of B7-CD28 interaction may cause unresponsiveness of T cells to subsequent exposure to Ag. Nevertheless, immunization by some B7- tumors induces an antitumor immune response. We found that the immune response against two B7- tumors, the mouse P815 mastocytoma and the E7C3 melanoma, requires host-derived B7, since blockage of the B7-CD28 interaction facilitates tumor growth and eliminates an antitumor response. B7 costimulation is provided in the regional, tumor-draining lymph nodes for the induction of a primary CTL response against both B7+ tumor and B7- tumor. However, the induction of a CTL response to B7+ tumors and its clonal expansion may occur at tumor sites in addition to secondary lymphoid organs so as to generate more effective tumor immunity.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Immunology|
|Publication status||Published - Jan 15 1997|
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