ICOS-deficient and ICOS YF mutant mice fail to control Toxoplasma gondii infection of the brain.

ABSTRACT: Resistance to chronic Toxoplasma gondii infection requires ongoing recruitment of T cells to the brain. Thus, the factors that promote, sustain, and regulate the T cell response to the parasite in the brain are of great interest. The costimulatory molecule ICOS (inducible T cell costimulator) has been reported to act largely through the PI3K pathway in T cells, and can play pro-inflammatory or pro-regulatory roles depending on the inflammatory context and T cell type being studied. During infection with T. gondii, ICOS promotes early T cell responses, while in the chronic stage of infection ICOS plays a regulatory role by limiting T cell responses in the brain. We sought to characterize the role of ICOS signaling through PI3K during chronic infection using two models of ICOS deficiency: to

SUBMITTER: O'Brien CA 

PROVIDER: S-EPMC6980566 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature