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Infection and Immunity, April 2006, p. 2382-2391, Vol. 74, No. 4
0019-9567/06/$08.00+0 doi:10.1128/IAI.74.4.2382-2391.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Departments of Microbiology and Immunology,1 Medicine, Faculty of Medicine, University of Montreal,2 Sainte-Justine Hospital,3 Laboratory of Molecular Biology, Clinical Research Institute of Montreal,4 Division of Experimental Medicine, McGill University, Montreal, Quebec, Canada5
Received 19 October 2005/ Returned for modification 21 December 2005/ Accepted 17 January 2006
Candida albicans causes oropharyngeal candidiasis (OPC) but rarely disseminates to deep organs in human immunodeficiency virus (HIV) infection. Here, we used a model of OPC in CD4C/HIVMut transgenic (Tg) mice to investigate the role of polymorphonuclear leukocytes (PMNs) and CD8+ T cells in limiting candidiasis to the mucosa. Numbers of circulating PMNs and their oxidative burst were both augmented in CD4C/HIVMutA Tg mice expressing rev, env, and nef of HIV type 1 (HIV-1), while phagocytosis and killing of C. albicans were largely unimpaired compared to those in non-Tg mice. Depletion of PMNs in these Tg mice did not alter oral or gastrointestinal burdens of C. albicans or cause systemic dissemination. However, oral burdens of C. albicans were increased in CD4C/HIVMutG Tg mice expressing only the nef gene of HIV-1 and bred on a CD8 gene-deficient background (CD8/), compared to control or heterozygous CD8+/ CD4C/HIVMutG Tg mice. Thus, CD8+ T cells contribute to the host defense against oral candidiasis in vivo, specifically in the context of nef expression in a subset of immune cells.
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