Next Article in Journal
Molecular Characterization of the Multidrug Resistant Escherichia coli ST131 Clone
Next Article in Special Issue
Elimination of Bloodstream Infections Associated with Candida albicans Biofilm in Intravascular Catheters
Previous Article in Journal
Environmental (Saprozoic) Pathogens of Engineered Water Systems: Understanding Their Ecology for Risk Assessment and Management
Previous Article in Special Issue
TLR-2 Signaling Promotes IL-17A Production in CD4+CD25+Foxp3+ Regulatory Cells during Oropharyngeal Candidiasis
Article Menu

Export Article

Open AccessReview
Pathogens 2015, 4(2), 406-421; doi:10.3390/pathogens4020406

Oropharyngeal Candidiasis in HIV Infection: Analysis of Impaired Mucosal Immune Response to Candida albicans in Mice Expressing the HIV-1 Transgene

1
Department of Microbiology, Infectious Diseases and Immunology, Faculty of Medicine, University of Montreal, C.P. 6128, succursale Centre-Ville, Montreal, PQ H3C 3J7, Canada
2
Laboratory of Molecular Biology, Clinical Research Institute of Montreal, 110, avenue des Pins Ouest, Montreal, PQ H2W 1R7, Canada
*
Author to whom correspondence should be addressed.
Academic Editor: Sarah Gaffen
Received: 23 May 2015 / Revised: 13 June 2015 / Accepted: 16 June 2015 / Published: 23 June 2015
(This article belongs to the Special Issue Candida Albicans Infections)
View Full-Text   |   Download PDF [1588 KB, uploaded 23 June 2015]   |  

Abstract

IL-17-producing Th17 cells are of critical importance in host defense against oropharyngeal candidiasis (OPC). Speculation about defective Th17 responses to oral C. albicans infection in the context of HIV infection prompted an investigation of innate and adaptive immune responses to Candida albicans in transgenic mice expressing the genome of HIV-1 in immune cells and displaying an AIDS-like disease. Defective IL-17 and IL-22-dependent mucosal responses to C. albicans were found to determine susceptibility to OPC in these transgenic mice. Innate phagocytes were quantitatively and functionally intact, and individually dispensable for control of OPC and to prevent systemic dissemination of Candida to deep organs. CD8+ T-cells recruited to the oral mucosa of the transgenic mice limited the proliferation of C. albicans in these conditions of CD4+ T-cell deficiency. Therefore, the immunopathogenesis of OPC in the context of HIV infection involves defective T-cell-mediated immunity, failure of crosstalk with innate mucosal immune effector mechanisms, and compensatory cell responses, which limit Candida infection to the oral mucosa and prevent systemic dissemination. View Full-Text
Keywords: Candidiasis; human immunodeficiency virus (HIV); AIDS; mucosal immunity; transgenic mice Candidiasis; human immunodeficiency virus (HIV); AIDS; mucosal immunity; transgenic mice
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

de Repentigny, L.; Goupil, M.; Jolicoeur, P. Oropharyngeal Candidiasis in HIV Infection: Analysis of Impaired Mucosal Immune Response to Candida albicans in Mice Expressing the HIV-1 Transgene. Pathogens 2015, 4, 406-421.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Pathogens EISSN 2076-0817 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top