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Induction of anti-tumor adaptive immunity by monoclonal antibodies. Tumor cells opsonized with antibodies are lysed through various effector mechanisms (Figure 1). Cell debris, apoptotic bodies, and antigen/antibody complexes are then captured by antigen-presenting cells (APCs) such as immature dendritic cells, leading to the activation of CD4+ T cells. Signal dangers are also involved in the sensing of tumor cells by APCs. CD4+ T cells trigger CD8+ cytotoxic T-cell and also likely B-cell activation, leading to the appearance of memory CD4+ and CD8+ T cells and likely memory B cells (not represented). This adaptive immunity opposes inhibitory mechanisms induced by tumor cells and by inflammation that parallels tumor growth. It counterbalances the role of regulatory T cells (Treg) and of immunosuppressive and/or pro-inflammatory cytokines (IL-10, IL-6…). Cross-presentation of tumor-associated antigens by APCs to CD8+ T cells as well as the presence of myeloid-derived suppressor cells (MDSC) such as M2 macrophages are not represented.

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