Interleukin 10 and dendritic cells are the main suppression mediators of regulatory T cells in human neurocysticercosis

Summary Neurocysticercosis is caused by the establishment of Taenia solium cysticerci in the central nervous system. It is considered that, during co‐evolution, the parasite developed strategies to modulate the host's immune response. The action mechanisms of regulatory T cells in controlling the immune response in neurocysticercosis are studied in this work. Higher blood levels of regulatory T cells with CD4 + CD45RO + forkhead box protein 3 (FoxP3) high and CD4 + CD25 high FoxP3 + CD95 high phenotype and of non‐regulatory CD4 + CD45RO + FoxP3 med T cells were found in neurocysticercosis patients with respect to controls. Interestingly, regulatory T cells express higher levels of cytotoxic T lymphocyte antigen 4 (CTLA‐4), lymphocyte‐activation gene 3 (LAG‐3), programmed death 1 (PD‐1) and glucocorticoid‐induced tumour necrosis factor receptor (GITR), suggesting a cell‐to‐cell contact mechanism with dendritic cells. Furthermore, higher IL‐10 and regulatory T cell type 1 (Tr1) levels were found in neurocysticercosis patients’ peripheral blood, suggesting that the action mechanism of regulatory T cells involves the release of immunomodulatory cytokines. No evidence was found of the regulatory T cell role in inhibiting the proliferative response. Suppressive regulatory T cells from neurocysticercosis patients correlated negatively with late activated lymphocytes (CD4 + CD38 + ). Our results suggest that, during neurocysticercosis, regulatory T cells could control the immune response, probably by a cell‐to‐cell contact with dendritic cells and interleukin (IL)‐10 release by Tr1, to create an immunomodulatory environment that may favour the development of T. solium cysticerci and their permanence in the central nervous system.