Abstract

BackgroundThe mechanisms through which allergies can be inhibited after preconception immunization with allergens are not fully understood. We aimed to evaluate whether maternal immunization can induce a regulatory B (B10) cell population in offspring in concert with allergy inhibition.MethodsC57BL/6 females were or were not immunized with OVA and were mated with normal WT males. Their offspring were evaluated at 3 days of age or 20 days after neonatal immunization. Human peripheral B cells from atopic and non-atopic individuals were also evaluated.ResultsPreconception OVA immunization induced B10 cells in offspring, and IL-10 production appeared to be critical for FcγRIIB upregulation in offspring B cells. Murine and human IL-10-producing B cells responded in vitro to IgG according to the atopic repertoire of the cells.ConclusionsOur results reveal that maternal immunization induces allergen-specific B10 cells in offspring and a pivotal role for the IgG repertoire in IL-10 production by murine and human B cells.

Highlights

  • The mechanisms through which allergies can be inhibited after preconception immunization with allergens are not fully understood

  • We found that the lung tissue infiltrating lymphocytes in the offspring from immunized mothers contained a higher amount of B cells that frequently produced IL-10 and expressed the B regulatory cells that produce IL-10 (B10) phenotype ­(CD19+IL-10+CD1dhigh; Fig. 1d) than those identified in the offspring from non-immunized mothers

  • A subsequent evaluation of the regulatory lymphocyte numbers on offspring spleens demonstrated that maternal OVA immunization substantially induced B10 cells in 3-day-old offspring, and this induction was maintained at 20 days of age after neonatal immunization (Fig. 1e)

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Summary

Introduction

The mechanisms through which allergies can be inhibited after preconception immunization with allergens are not fully understood. Our group has studied type I hypersensitivity inhibition in murine models for the last decade [1,2,3,4,5,6,7] During this period, we proposed that maternal IgG can play a pivotal role in offspring immune modulation, but the mechanisms underlying this phenomenon were not fully elucidated. In the 90s, it was revealed that maternal antibodies are passively transferred to offspring during the gestational and weaning periods These antibodies, IgG, can interact directly with the offspring’s immune system, even in the absence of antigens [8], and might involve maternal antibody-allergen immune complexes that directly interact with the inhibitory receptor. FcγRIIb (CD32b) expressed by offspring B cells [9] These interactions can in turn regulate the production of IgE antibodies, inhibiting the development of allergies. Because the main event of allergy inhibition is the control of IgE production by B cells, we believe that this population plays a pivotal role as the subject of the effects induced by maternal immunization

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