Role of fibrosarcoma-induced CD11b(+) myeloid cells and tumor necrosis factor-alpha in B cell responses

The role of B cells in the anti-tumor immune response remains controversial. An increase in the number of B cells in the peripheral blood of some tumor patients has been associated with poor immunotherapy efficacy. However, the mechanism leading to the generation of these cells is not well-described. Using a fibrosarcoma model, we show that intraperitoneal administration of a xenogeneic antigen in tumor-bearing mice evokes large increases in antigen-specific serum immunoglobulin formation compared to tumor-naive mice. An inability of tumor-bearing mice to induce enhanced antibody production after myeloid cell depletion suggests the antibody responses are CD11b(+) myeloid cell-dependent. In vitro, CD11b(+) myeloid cells promoted B cell proliferation, activation, and survival. High levels of tumor necrosis factor (TNF)-alpha were produced by CD11b(+) cells, and TNF-alpha blockade inhibited B cell responses. CD11b(+) cells appear to be important promoters of B cell responses and targeting B cells may increase the efficacy of immunotherapy in tumor-bearing hosts.

Automated summary

The role of B cells in the anti-tumor immune response is controversial. An increase in the number of B cells in the peripheral blood of some tumor patients has been associated with poor immunotherapy efficacy. This study suggests that CD11b(+) myeloid cells promote B cell proliferation, activation, and survival, and targeting B cells may increase the efficacy of immunotherapy in tumor-bearing hosts.