γ/δ T cell-deficient mice exhibit reduced disease severity and decreased inflammatory response in the brain in murine neurocysticercosis

In a recently developed mouse model for neurocysticercosis, the immune response was characterized by a massive influx of gammadelta T cells and a type 1 pathway of cytokine expression. To understand the role of gammadelta T cells during this infection, the cellular and cytokine response was analyzed in mice that lack gammadelta T cells (TCRdelta(-/-)). In TCRdelta(-/-) mice, Mesocestoides cord metacestodes preferentially invaded the extraparenchymal areas of the brain. Furthermore, parasites were able to escape from the brain and establish a systemic infection with liver and peritoneal involvement. Immunopathological studies indicated that TCRdelta(-/-) mice develop little inflammatory response and less neurological symptomatology. Significantly reduced numbers of T cells, macrophages, dendritic cells, and mast cells were present in the brain. The cytokine response in the brain of TCRdelta(-/-) mice appears to be a mixed type1/type 2 response with low levels of IL-2, IL-4, IL-10, IL-12, IL-13, IL-15, and IFN-gamma. To further investigate the immunological significance of this cell population, gammadelta T cells were adoptively transferred into intracranially infected TCRdelta(-/-) mice. gammadelta T cells were specifically recruited into the CNS in response to this parasitic infection, and they were able to target the infected brain within 12 h after transfer. These results suggest that gammadelta T cells are key players in the immune response elicited during this CNS infection and direct a type 1 response in wild-type mice upon infection.