Candida albicans and Candida parapsilosis induce different T-cell responses in human peripheral blood mononuclear cells

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Publication year
2013Source
The Journal of Infectious Diseases, 208, 4, (2013), pp. 690-698ISSN
Publication type
Article / Letter to editor

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Organization
Radiology
Internal Medicine
Journal title
The Journal of Infectious Diseases
Volume
vol. 208
Issue
iss. 4
Page start
p. 690
Page end
p. 698
Subject
N4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity; ONCOL 5: Aetiology, screening and detectionAbstract
Candida parapsilosis is the third most frequent cause of candidemia. Despite its clinical importance, little is known about the human immunological response to C. parapsilosis. In this study, we compared the cytokine responses evoked by Candida albicans and C. parapsilosis. C. parapsilosis-stimulated human peripheral blood mononuclear cells (PBMCs) produced similar quantities of tumor necrosis factor alpha and interleukin 6 and slightly lower amounts of interleukin 1beta, compared with C. albicans-stimulated cells. PBMCs stimulated with C. parapsilosis displayed a skewed T-helper cell response, producing more interleukin 10 and less interferon gamma than cells stimulated with C. albicans. Notably, C. parapsilosis induced much less interleukin 17 and interleukin 22 production as compared to C. albicans. Inhibition of the 3 classical mitogen-activated protein kinases (p38 kinase, ERK, and JNK) revealed kinase-dependent differences in reductions in cytokine production by the 2 Candida species. Decreased cytokine production after inhibition of dectin 1 revealed that this receptor plays a major role in the recognition of both C. albicans and C. parapsilosis. These data improve understanding of the immune response triggered by C. parapsilosis, a first step for the future design of immunotherapeutic strategies for these infections.
This item appears in the following Collection(s)
- Academic publications [202801]
- Electronic publications [100942]
- Faculty of Medical Sciences [80020]
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