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Schistosome-induced pulmonary B cells inhibit allergic airway inflammation and display a reduced Th2-driving function.
van der Vlugt, L E P M Obieglo, K Ozir-Fazalalikhan, A Haeberlein, S Smits, H H
van der Vlugt, L E P M
Obieglo, K
Ozir-Fazalalikhan, A
Haeberlein, S
Smits, H H
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2017-08
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Abstract
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.
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Schistosome-induced pulmonary B cells inhibit allergic airway inflammation and display a reduced Th2-driving function. 2017, 47 (9):545-554 Int. J. Parasitol.
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en
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1879-0135