| First Author | Habener A | Year | 2017 |
| Journal | Eur J Immunol | Volume | 47 |
| Issue | 3 | Pages | 552-562 |
| PubMed ID | 27995616 | Mgi Jnum | J:249512 |
| Mgi Id | MGI:5923524 | Doi | 10.1002/eji.201646518 |
| Citation | Habener A, et al. (2017) B cell subsets are modulated during allergic airway inflammation but are not required for the development of respiratory tolerance in a murine model. Eur J Immunol 47(3):552-562 |
| abstractText | 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 (muMT) 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, muMT 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. |
