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Infection and Immunity, December 2003, p. 7159-7163, Vol. 71, No. 12
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.12.7159-7163.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Shiguang Huang,1,3,
and Lloyd H. Kasper1*
Department of Medicine and Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756,1 Sun Yat-sen University School of Medicine, Guangzhou 510089,2 Jinan University School of Medicine, Guangzhou 510632, China3
Received 14 July 2003/ Returned for modification 10 August 2003/ Accepted 16 September 2003
To understand the role of interleukin-10 (IL-10) in ocular toxoplasmosis, we compared C57BL/6 (B6) and BALB/c background mice lacking a functional IL-10 gene (IL-10-/-) and B6 transgenic mice expressing IL-10 under the control of the IL-2 promoter. Increased cellular infiltration and necrosis were observed in the eye tissue of IL-10-/- mice of both the B6 and BALB/c backgrounds with associated changes in the levels of cytokines in serum. In contrast, there was no evidence of necrosis in the eye tissue from IL-10 transgenic mice following parasite exposure. Our results demonstrate that IL-10 is important in the regulation of inflammation during acute ocular toxoplasmosis.
Present address: Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0425.
Present address: Jinan University School of Medicine, Guangzhou 510632, China.
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