Cd8+ T Cells but Not Polymorphonuclear Leukocytes Are Required to Limit Chronic Oral Carriage of Candida Albicans in Transgenic Mice Expressing Human Immunodeficiency Virus Type 1.
From: Department of Microbiology and Immunology, Sainte-Justine Hospital and University of Montreal, 3175 Côte Ste-Catherine, Montreal, Quebec H3T 1C5, Canada.
Infection and immunity
- Publish Date: Apr 2006
- ISSN: 0019-9567
- Volume: 74
- Issue: 4
- Pages: 2382-91
- Medium: Print
- Language: English
- Citation (JAMA): Marquis Miriam, Lewandowski Daniel, Dugas Véronique, et al. Cd8+ T Cells but Not Polymorphonuclear Leukocytes Are Required to Limit Chronic Oral Carriage of Candida Albicans in Transgenic Mice Expressing Human Immunodeficiency Virus Type 1.. Infect. Immun. Apr 2006;74:2382-91
Abstract
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/HIV(Mut) 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/HIV(MutA) 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/HIV(MutG) 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/HIV(MutG) 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.
Mesh Headings (Keywords): Animals, Antigens, CD4, Antigens, CD8, CD8-Positive T-Lymphocytes, Candida albicans, Candidiasis, Oral, Cells, Cultured, Chronic Disease, Disease Models, Animal, Female, HIV Infections, HIV-1, Humans, Leukopenia, Male, Mice, Mice, Inbred C3H, Mice, Knockout, Mice, Transgenic, Neutrophils, Phagocytosis, Respiratory Burst, Time Factors
Check for Full Text / PubMed Unique Identifier (PMID): 16552068
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.