B cell subsets are modulated during allergic airway inflammation but are not required for the development of respiratory tolerance in a murine model

Allergic asthma is a widespread chronic inflammatory disease of the airways. The role of different B cell subsets in developing asthma and respiratory tolerance is not well known. Especially regulatory B (Breg) cells are proposed to be important in asthma regulation. Using wild‐type (WT) and B cell‐deficient (μMT) mice we investigated how B cells are affected by induction of allergic airway inflammation and respiratory tolerance and whether they are necessary to develop these conditions. WT mice with an asthma‐like phenotype, characterized by increased airway hyper reactivity, eosinophilic airway inflammation, mucus hypersecretion and elevated Th2 cytokines, exhibited increased MHCII and CD23 expression on follicular mature B cells in lung, bronchial lymph nodes (bLN) and spleen, which contributed to allergen‐specific T cell proliferation in vitro. Germinal center B cell numbers were elevated and associated with increased production of allergen‐specific immunoglobulins especially in bLN. In contrast, respiratory tolerance clearly attenuated these B cell alterations and directly enhanced marginal zone precursor B cells, which induced regulatory T cells in vitro. However, μMT mice developed asthma‐like and tolerized phenotypes like WT mice. Our data indicate that although B cell subsets are affected by asthma‐like and respiratory tolerant phenotypes, B cells are not required for tolerance induction.