[Frontiers in Bioscience 14, 1970-1978, January 1, 2009]

IFN-γ in Candida albicans infections

Daniel Gozalbo, Maria Luisa Gil

Departamento de Microbiologia y Ecología, Universitat de Valencia, 46100 Burjasot, Valencia, Spain

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Interferon-gamma (IFN-γ)
4. IFN-γ in Candida albicans infections
4.1. IFN-γ is essential for host defence against invasive candidiasis
4.2. IFN-γ production by NK cells
4.3. IFN-γ production by Th1 cells
4.4. IFN-γ production by γδ T cells / CD8 T cells
5. Perspective
6. Acknowledgements
7. References

1. ABSTRACT

The dimorphic fungus Candida albicans is the most frequent etiologic agent that causes opportunistic infections called candidiasis, a disease whose systemic manifestation could prove fatal and whose incidence is increasing as a result of an expanding immunocompromised population. Here we review the role of interferon-gamma (IFN-g ) in the host protection against invasive candidiasis. This cytokine plays an essential role in both the innate and adaptive arms of the immune response to candidiasis. We focus on recent progress on host-pathogen interactions at the molecular level, leading to the production of IFN-g by host cells. IFN-g is produced by CD4 Th1, CD8, γδ T, and natural killer (NK) cells, essentially in response to both IL-12 and/or IL-18, and plays an important role in the regulation of the immune system as well as in the control of the infectious process. IFN-g is required for optimal activation of phagocytes, collaborates in the generation of protective antibody response, and favours the development of a Th1 protective response.