B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation

Candida albicans is usually a benign member of the human gut microbiota, but can become pathogenic under certain circumstances, for example in an immunocompromised host. The innate immune system, in particular neutrophils and macrophages, constitutes a crucial first line of defense against fungal in...

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Autores principales: Marta Ferreira-Gomes, Melissa Wich, Sally Böde, Bernhard Hube, Ilse D. Jacobsen, Berit Jungnickel
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/6aaafc550f1c43f093d4748663671e7b
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spelling oai:doaj.org-article:6aaafc550f1c43f093d4748663671e7b2021-11-08T05:55:26ZB Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation1664-322410.3389/fimmu.2021.698849https://doaj.org/article/6aaafc550f1c43f093d4748663671e7b2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.698849/fullhttps://doaj.org/toc/1664-3224Candida albicans is usually a benign member of the human gut microbiota, but can become pathogenic under certain circumstances, for example in an immunocompromised host. The innate immune system, in particular neutrophils and macrophages, constitutes a crucial first line of defense against fungal invasion, however adaptive immunity may provide long term protection and thus allow vaccination of at risk patients. While TH1 and TH17 cells are important for antifungal responses, the role of B cells and antibodies in protection from C. albicans infection is less well defined. In this study, we show that C. albicans hyphae but not yeast, as well as fungal cell wall components, directly activate B cells via MyD88 signaling triggered by Toll- like receptor 2, leading to increased IgG1 production. While Dectin-1 signals and specific recognition by the B cell receptor are dispensable for B cell activation in this system, TLR2/MyD88 signals cooperate with CD40 signals in promoting B cell activation. Importantly, recognition of C. albicans via MyD88 signaling is also essential for induction of IL-6 secretion by B cells, which promotes TH17 polarization in T-B cell coculture experiments. B cells may thus be activated directly by C. albicans in its invasive form, leading to production of antibodies and T cell help for fungal clearance.Marta Ferreira-GomesMelissa WichSally BödeBernhard HubeBernhard HubeIlse D. JacobsenIlse D. JacobsenBerit JungnickelFrontiers Media S.A.articleCandida albicansB cellstoll-like receptorsIL-6TH17 cellsfungal cell wallImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic Candida albicans
B cells
toll-like receptors
IL-6
TH17 cells
fungal cell wall
Immunologic diseases. Allergy
RC581-607
spellingShingle Candida albicans
B cells
toll-like receptors
IL-6
TH17 cells
fungal cell wall
Immunologic diseases. Allergy
RC581-607
Marta Ferreira-Gomes
Melissa Wich
Sally Böde
Bernhard Hube
Bernhard Hube
Ilse D. Jacobsen
Ilse D. Jacobsen
Berit Jungnickel
B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation
description Candida albicans is usually a benign member of the human gut microbiota, but can become pathogenic under certain circumstances, for example in an immunocompromised host. The innate immune system, in particular neutrophils and macrophages, constitutes a crucial first line of defense against fungal invasion, however adaptive immunity may provide long term protection and thus allow vaccination of at risk patients. While TH1 and TH17 cells are important for antifungal responses, the role of B cells and antibodies in protection from C. albicans infection is less well defined. In this study, we show that C. albicans hyphae but not yeast, as well as fungal cell wall components, directly activate B cells via MyD88 signaling triggered by Toll- like receptor 2, leading to increased IgG1 production. While Dectin-1 signals and specific recognition by the B cell receptor are dispensable for B cell activation in this system, TLR2/MyD88 signals cooperate with CD40 signals in promoting B cell activation. Importantly, recognition of C. albicans via MyD88 signaling is also essential for induction of IL-6 secretion by B cells, which promotes TH17 polarization in T-B cell coculture experiments. B cells may thus be activated directly by C. albicans in its invasive form, leading to production of antibodies and T cell help for fungal clearance.
format article
author Marta Ferreira-Gomes
Melissa Wich
Sally Böde
Bernhard Hube
Bernhard Hube
Ilse D. Jacobsen
Ilse D. Jacobsen
Berit Jungnickel
author_facet Marta Ferreira-Gomes
Melissa Wich
Sally Böde
Bernhard Hube
Bernhard Hube
Ilse D. Jacobsen
Ilse D. Jacobsen
Berit Jungnickel
author_sort Marta Ferreira-Gomes
title B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation
title_short B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation
title_full B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation
title_fullStr B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation
title_full_unstemmed B Cell Recognition of Candida albicans Hyphae via TLR 2 Promotes IgG1 and IL-6 Secretion for TH17 Differentiation
title_sort b cell recognition of candida albicans hyphae via tlr 2 promotes igg1 and il-6 secretion for th17 differentiation
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/6aaafc550f1c43f093d4748663671e7b
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