¹Department of Molecular Microbiology and Immunology, Brown University, Providence, RI, USA

Correspondence: Dr GS Yap, Department of Molecular Microbiology and Immunology, Brown University, Box G-B6, Providence, RI 02912, USA. E-mail: George_Yap@Brown.edu

Received 21 November 2006; Accepted 23 November 2006; Published online 16 January 2007.

Abstract

Toxoplasma gondii infection is an important cause of central nervous system and ocular disease, both in immunocompromised and in certain immunocompetent populations. Although parasite-mediated host cell lysis is probably the principal cause of tissue destruction in immunodeficiency states, hypersensitivity and inflammatory responses may underlie severe disease in otherwise immuno-sufficient individuals. In this review, we have critically evaluated the body of experimental evidence indicating a role of CD4 T cells in systemic and local immunopathology associated with T. gondii infection. We also discuss the pathogenic roles of cytokines produced by T helper (Th) 1 and Th17 cells and the protective and homeostatic roles of interleukin (IL)-10, transforming growth factor- and IL-27 in modulating hypersensitivity responses induced by T. gondii.