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CD24hiCD27+ B cells from patients with allergic asthma have impaired regulatory activity in response to lipopolysaccharide




Regulatory B cells have been identified that strongly reduce allergic and auto-immune inflammation in experimental models by producing IL-10. Recently, several human regulatory B-cell subsets with an impaired function in auto-immunity have been described, but there is no information on regulatory B cells in allergic asthma.


In this study, the frequency and function of IL-10 producing B-cell subsets in allergic asthma were investigated.


Isolated peripheral blood B cells from 13 patients with allergic asthma and matched healthy controls were analyzed for the expression of different regulatory B-cell markers. Next, the B cells were activated by lipopolysaccharide (LPS), CpG or through the B-cell receptor, followed by co-culture with endogenous memory CD4+ T cells and house dust mite allergen DerP1.


Lower number of IL-10 producing B cells were found in patients in response to LPS, however, this was not the case when B cells were activated through the B-cell receptor or by CpG. Further dissection showed that only the CD24hiCD27+ B-cell subset was reduced in number and IL-10 production to LPS. In response to DerP1, CD4+ T cells from patients co-cultured with LPS-primed total B cells produced less IL-10 compared to similar cultures from controls. These results are in line with the finding that sorted CD24hiCD27+ B cells are responsible for the induction of IL-10+ CD4+ T cells.


Taken together, these data indicate that CD24hiCD27+ B cells from allergic asthma patients produce less IL-10 in response to LPS leading to a weaker IL-10 induction in T cells in response to DerP1, which may play a role in allergic asthma.