CC chemokines mediate leukocyte trafficking into the central nervous system during murine neurocysticercosis:: Role of γδ T cells in amplification of the host immune response

According to a previous report, the degree of the host immune response highly correlates with severity of the disease in the murine model for neurocysticercosis. In wild-type mice, Mesocestoides corti infection induced a rapid and extensive accumulation of gammadelta T cells and macrophages in the brain. NK cells, dendritic cells, alphabeta T cells, and B cells were also recruited to the brain but at lower levels. In contrast, gammadelta T-cell-deficient mice exhibited decreased cellular infiltration and reduced central nervous system (CNS) pathology. To understand the mechanisms of leukocyte recruitment into the CNS, chemokine expression was analyzed in infected brains in the present study. MCP-1 (CCL2), MIP-1alpha (CCL3), and MIP-1beta (CCL4) were up-regulated within 2 days after M. cord infection. Protein expression of RANTES (CCL5), eotaxin (CCL11), and MIP-2 was detected later, at 1 week postinfection. Correlating with the decreased cellular infiltration, delta chain T-cell receptor-deficient (TCRdelta(-/-)) mice exhibited substantially reduced levels of most of the chemokines analyzed (with the exception of eotaxin). The results suggest that gammadelta T cells play an important role in the CNS immune response by producing chemokines such as MCP-1 and MIP-1alpha, enhancing leukocyte trafficking into the brain during murine neurocysticercosis.