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, 2017 03.
Article
in En
| MEDLINE
| ID: mdl-27995616
ABSTRACT
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.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
Pneumonia
/
Respiratory Hypersensitivity
/
Asthma
/
B-Lymphocyte Subsets
/
T-Lymphocytes, Regulatory
/
Th2 Cells
/
B-Lymphocytes, Regulatory
Limits:
Animals
/
Humans
Language:
En
Year:
2017
Type:
Article