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Molecules 2018, 23(9), 2339;

The Response of IL-17-Producing B Cells to ArtinM Is Independent of Its Interaction with TLR2 and CD14

Departamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP 14049-900, Brazil
Author to whom correspondence should be addressed.
Received: 30 July 2018 / Revised: 28 August 2018 / Accepted: 29 August 2018 / Published: 13 September 2018
(This article belongs to the Special Issue Immunomodulatory Compounds)
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ArtinM, a d-mannose-binding lectin from Artocarpus heterophyllus, activates antigen-presenting cells by recognizing Toll-like receptor (TLR)2 and cluster of differentiation (CD)14 N-glycans, induces cytokine production, and promotes type 1 T helper (Th1) immunity, a process that plays an assisting role in the combat against fungal infections. We recently demonstrated that ArtinM stimulates CD4+ T cells to produce interleukin (IL)-17 through direct interaction with CD3. Here, we further investigated the effects of ArtinM on the production of IL-17 by B cell activation. We showed that ArtinM activates murine B cells, increasing IL-17 and IL-12p40 production. The direct effect of ArtinM was sufficient to induce IL-17 production in B cells, and we did not find differences in the levels of IL-17 between the B cells purified from the wild-type (WT) and knockout (KO) mice for TLR2 or CD14 in the presence of ArtinM. Thus, the effects of ArtinM on splenic B cells through carbohydrate recognition may contribute to Th17 immunity; however, the mechanism involved is not associated with the interaction of ArtinM with TLR2 and CD14. The current work represents a pioneering effort in the understanding of the induction of IL-17 by lectins in B cells. View Full-Text
Keywords: IL-17; B cells; ArtinM; TLR2; CD14; carbohydrate recognition IL-17; B cells; ArtinM; TLR2; CD14; carbohydrate recognition

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Oliveira-Brito, P.K.M.; Roque-Barreira, M.C.; da Silva, T.A. The Response of IL-17-Producing B Cells to ArtinM Is Independent of Its Interaction with TLR2 and CD14. Molecules 2018, 23, 2339.

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