Abstract The role of B lymphocytes in the pathogenesis and treatment of cancer has not received as much attention as the role of T cells. However, most patients with solid tumors harbor circulating antitumor antibodies and most tumors contain a population of infiltrating B cells implying an association between oncogenic events and B-cell activation. B-cell immunity can be beneficial by providing antibody-mediated protection from oncogenic viruses or a source of recombinant tumor-specific antibodies that can be used in combination with chemotherapeutic regimens. However, activation of B cells may also be detrimental to an effective antitumor response. Tumor-reactive antibodies and B cells often recognize antigens that are generated during the unscheduled apoptotic and necrotic death processes, which accompany tumor progression and may be involved in wound-healing processes that promote tumor growth and impair protective T-cell responses. Therefore, methods to eliminate autoreactive B cells, or switch them to a B effector-1 (Be-1) phenotype that amplifies Th1/Tc1-type T-cell responses, which are typically associated with effective antitumor responses, may improve the clinical outcomes of T-cell-mediated immunotherapies. Possible strategies include the administration of B-celldepleting monoclonal antibodies, use of targeted B-cell stimulatory agents such as Toll-like Receptor agonists, and adoptive transfer of large numbers of ex vivo generated tumor-reactive Be-1 cells
