CD8+ T Cell Immunity is Compromised by Anti-CD20 Treatment and Rescued by Interleukin-17A.

Monoclonal antibody targeting the CD20 antigen on B cells is used to treat the majority of non-Hodgkin lymphoma patients and some autoimmune disorders. This therapy generates adverse effects, notably opportunistic infections and activation of viruses from latency. Here, using the infection murine model with the intracellular parasiteTrypanosoma cruzi, we report that anti-CD20 treatment affects not only B cell responses but also CD8+T cell responses, representing the most important immune effectors involved in control of intracellular pathogens. Anti-CD20 treatment, directly or indirectly, affects cytotoxic T cell number and function, and this deficient response was rescued by the cytokine IL-17A. The identification of IL-17A as the cytokine capable of reversing the poor response of CD8+T cells provides information about a potential therapeutic treatment aimed at enhancing defective immunity induced by B cell depletion.