Role of host antigen receptor-bearing and antigen receptor-negative cells in immune response to rat adenocarcinoma 13762.

Involvement of individual immune cell populations in the immune response to rat breast adenocarcinoma 13762 was studied by selective depletion treatments in vivo. Depletion of Ag nonspecific host defense cells from naive animals before tumor challenge resulted in statistically significant acceleration of tumor growth (p less than 0.01 or less), whereas depletion of either CD4+ T cells or CD8+ T cells had no effect on the incidence or kinetics of tumor development. In contrast to naive animals treated before tumor challenge, animals actively immunized by injection of irradiated tumor before depleting treatments were shown to require CD4+ T cells to reject tumorigenic challenge. Depletion of either macrophages or neutrophils from immune animals also increased tumor development, whereas NK cells were not involved. Depletion of CD8+ T cells from immune animals permitted transient growth of tumors that were subsequently rejected, implying a role in tumor rejection. Transfer of immune antiserum to naive animals at the time of tumor challenge was without effect on tumor development. Depletion of CD4+ T cells, neutrophils, or macrophages in the priming phase of antitumor immune response abrogated tumor immunity, but depletion of CD8+ T cells or NK cells was without effect on the ability to prime animals by immunization with irradiated cells. Collectively, these data suggest that host natural defense cells that do not express Ag receptor are primarily responsible for resistance of adenocarcinoma 13762 growth in naive animals. In contrast, tumor immunity induced by active immunization requires Ag receptor-bearing CD4+ T cells and involves participation of CD8+ T cells, neutrophils, or macrophages in elimination of tumor.