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The role of the IL-12 cytokine family in directing T-cell responses in oral candidosis.

Wei XQ, Rogers H, Lewis MA, Williams DW - Clin. Dev. Immunol. (2010)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Cardiff University, Heath Park, UK. weix1@cardiff.ac.uk

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.

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Related in: MedlinePlus

Peripheral blood monocytes from a healthy individual responded to C. albicans stimulation for Th1 cytokine (IFNγ) production, Th17 cytokine (IL-17) production, but not Th2 cytokine (IL-4) production. The cytokines were measured with CBA kit (BD bioscience).
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fig3: Peripheral blood monocytes from a healthy individual responded to C. albicans stimulation for Th1 cytokine (IFNγ) production, Th17 cytokine (IL-17) production, but not Th2 cytokine (IL-4) production. The cytokines were measured with CBA kit (BD bioscience).

Mentions: T-cell responses can be generated by coculture of a pathogen's antigen with peripheral blood monocytes. After several days of culture, the antigen-specific T-cells can be recalled to produce cytokines, such as the Th1 cell cytokine IFNγ [90]. We have isolated human PBMC from a healthy donor and recalled the T-cell response using heat killed C. albicans. Predominant Th1 and Th17 responses based on the cytokine profiles were seen at days 1, 3, and 7 after culturing PBMC with heat killed C. albicans (Figure 3).


The role of the IL-12 cytokine family in directing T-cell responses in oral candidosis.

Wei XQ, Rogers H, Lewis MA, Williams DW - Clin. Dev. Immunol. (2010)

Peripheral blood monocytes from a healthy individual responded to C. albicans stimulation for Th1 cytokine (IFNγ) production, Th17 cytokine (IL-17) production, but not Th2 cytokine (IL-4) production. The cytokines were measured with CBA kit (BD bioscience).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2963117&req=5

fig3: Peripheral blood monocytes from a healthy individual responded to C. albicans stimulation for Th1 cytokine (IFNγ) production, Th17 cytokine (IL-17) production, but not Th2 cytokine (IL-4) production. The cytokines were measured with CBA kit (BD bioscience).
Mentions: T-cell responses can be generated by coculture of a pathogen's antigen with peripheral blood monocytes. After several days of culture, the antigen-specific T-cells can be recalled to produce cytokines, such as the Th1 cell cytokine IFNγ [90]. We have isolated human PBMC from a healthy donor and recalled the T-cell response using heat killed C. albicans. Predominant Th1 and Th17 responses based on the cytokine profiles were seen at days 1, 3, and 7 after culturing PBMC with heat killed C. albicans (Figure 3).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Cardiff University, Heath Park, UK. weix1@cardiff.ac.uk

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.

Show MeSH
Related in: MedlinePlus