Schistosome-induced pulmonary B cells inhibit allergic airway inflammation and display a reduced Th2-driving function.
Autor: | van der Vlugt LEPM; Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands; Current address: Department of Internal Medicine-Rheumatology, University of Michigan Medical School, 109 Zina Pitcher Place, Ann Arbor, MI, USA., Obieglo K; Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands., Ozir-Fazalalikhan A; Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands., Sparwasser T; Institute of Infection Immunology, Twincore/Centre for Experimental and Clinical Infection Research, Feodor-Lynen-Straße 7, 30625 Hanover, Germany., Haeberlein S; Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands; Current address: Institute for Parasitology, Justus-Liebig-University Giessen, Schubertstrasse 81, Giessen, Germany., Smits HH; Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. Electronic address: H.H.Smits@lumc.nl. |
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Jazyk: | angličtina |
Zdroj: | International journal for parasitology [Int J Parasitol] 2017 Aug; Vol. 47 (9), pp. 545-554. Date of Electronic Publication: 2017 Apr 04. |
DOI: | 10.1016/j.ijpara.2017.02.002 |
Abstrakt: | Chronic schistosome infections protect against allergic airway inflammation (AAI) via the induction of IL-10-producing splenic regulatory B (Breg) cells. Previous experiments have demonstrated that schistosome-induced pulmonary B cells can also reduce AAI, but act independently of IL-10. We have now further characterized the phenotype and inhibitory activity of these protective pulmonary B cells. We excluded a role for regulatory T (Treg) cell induction as putative AAI-protective mechanisms. Schistosome-induced B cells showed increased CD86 expression and reduced cytokine expression in response to Toll-like receptor (TLR) ligands compared with control B cells. To investigate the consequences for T cell activation we cultured ovalbumin (OVA)-pulsed, schistosome-induced B cells with OVA-specific transgenic T cells and observed less Th2 cytokine expression and T cell proliferation compared with control conditions. This suppressive effect was preserved even under optimal T cell stimulation by anti-CD3/28. Blocking of the inhibitory cytokines IL-10 or TGF-β only marginally restored Th2 cytokine induction. These data suggest that schistosome-induced pulmonary B cells are impaired in their capacity to produce cytokines to TLR ligands and to induce Th2 cytokine responses independent of their antigen-presenting function. These findings underline the presence of distinct B cell subsets with different stimulatory or inhibitory properties even if induced by the same type of helminth. (Copyright © 2017 Australian Society for Parasitology. Published by Elsevier Ltd. All rights reserved.) |
Databáze: | MEDLINE |
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