The Role of the IL-12 Cytokine Family in Directing T-Cell Responses in Oral Candidosis

Wei, Xiao-Qing ORCID: https://orcid.org/0000-0002-6274-8503, Rogers, Helen, Lewis, Michael Alexander Oxenham ORCID: https://orcid.org/0000-0003-1917-0651 and Williams, David Wynne ORCID: https://orcid.org/0000-0002-7351-5131 2011. The Role of the IL-12 Cytokine Family in Directing T-Cell Responses in Oral Candidosis. Clinical & Developmental Immunology , 697340. 10.1155/2011/697340

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Abstract

Candida albicans is an opportunistic fungal pathogen that normally exists as a harmless commensal in humans. In instances where host debilitation occurs, Candida can cause a range of clinical infections, and whilst these are primarily superficial, effecting mucosal membranes, systemic infections can develop in severely immunocompromised individuals. The mechanism of host immunity during commensal carriage of C. albicans has been intensively studied. In this paper, we present the most recent information concerning host recognition of C. albicans leading to cytokine production and the subsequent T-cell responses generated in response to C. albicans. Particular focus is given to the role of the IL-12 cytokine family including IL-12, IL-23, IL-27, and IL-35, in host immunity to Candida. CD4(+) T-cells are considered crucial in the regulation of immunity and inflammation. In this regard, the role of Th1/2, helper cells, together with the recently identified Th17 and Treg cells in candidosis will be discussed. Understanding the detailed mechanisms that underlie host immunity to Candida not only will be of benefit in terms of the infections caused by this organism but could also be exploited in the development of therapeutic interventions for other diseases.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Dentistry
Additional Information:	10 pp.
Publisher:	Hindawi Publishing Corporation
ISSN:	1740-2522
Date of First Compliant Deposit:	30 March 2016
Last Modified:	04 Oct 2023 09:22
URI:	https://orca.cardiff.ac.uk/id/eprint/16110

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