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Ocular toxoplasmosis (OT) can occur in the children of mothers infected with Toxoplasma gondii during pregnancy. It is not limited to the congenitally infected, but can also occur following adult-acquired infection or as a result of disease reactivation in immune-compromised and pregnant individuals. Many aspects of immune privilege in the eye, including constitutive TGF-beta expression and reduced MHC class 1 expression, would appear at first to favour parasite survival. Conversely, many of the mechanisms that control parasite multiplication in other anatomical sites, such as nitric oxide expression, IFN-gamma and TNF-alpha, are known to disrupt immune privilege and are associated with ocular damage. Taking into account the opposing needs of limiting parasite multiplication and minimizing tissue destruction we review the pathogenesis of OT in the murine model.

Original publication

DOI

10.1111/j.1365-3024.2006.00874.x

Type

Journal

Parasite immunology

Publication Date

12/2006

Volume

28

Pages

635 - 642

Addresses

Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, UK.

Keywords

Animals, Mice, Inbred BALB C, Mice, Inbred C57BL, Humans, Mice, Toxoplasma, Toxoplasmosis, Ocular, Disease Models, Animal, Pregnancy, Female