B lymphocytes can be activated to act as antigen presenting cells to promote anti-tumor responses.

Immune evasion by tumors includes several different mechanisms， including the inefficiency of antigen presenting cells (APCs) to trigger anti-tumor T cell responses. B lymphocytes may display a pro-tumoral role but can also be modulated to function as antigen presenting cells to T lymphocytes， capable of triggering anti-cancer immune responses. While dendritic cells， DCs， are the best APC population to activate naive T cells， DCs or their precursors， monocytes， are frequently modulated by tumors， displaying a tolerogenic phenotype in cancer patients. In patients with cervical cancer， we observed that monocyte derived DCs are tolerogenic， inhibiting allogeneic T cell activation compared to the same population obtained from patients with precursor lesions or cervicitis. In this work， we show that B lymphocytes from cervical cancer patients respond to treatment with sCD40L and IL-4 by increasing the CD80+CD86+ population， therefore potentially increasing their ability to activate T cells. To test if B lymphocytes could actually trigger anti-tumor T cell responses， we designed an experimental model where we harvested T and B lymphocytes， or dendritic cells， from tumor bearing donors， and after APC stimulation， transplanted them， together with T cells into RAG1-/- recipients， previously injected with tumor cells. We were able to show that anti-CD40 activated B lymphocytes could trigger secondary T cell responses， dependent on MHC-II expression. Moreover， we showed that dendritic cells were resistant to the anti-CD40 treatment and unable to stimulate anti-tumor responses. In summary， our results suggest that B lymphocytes may be used as a tool for immunotherapy against cancer.