IFNγ-Producing B Cells Play a Regulating Role in Infection-Mediated Inhibition of Allergy
by
,
Sai Qiao
1,2,3,†
,
Ying Peng
1,2,†,
Chunyan Zhang
1,2,
Rony Thomas
1,2,
Shuhe Wang
1,2 and
Xi Yang
1,2,* 1
Department of Immunology, Rady Max College of Medicine, University of Manitoba, Winnipeg, MB R3E 0T5, Canada
2
Department of Medical Microbiology and Infectious Diseases, Rady Max College of Medicine, University of Manitoba, Winnipeg, MB R3E 0T5, Canada
3
Department of Clinical Laboratory, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, China
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Biology 2023, 12(9), 1259; https://doi.org/10.3390/biology12091259
Submission received: 1 August 2023
/
Revised: 13 September 2023
/
Accepted: 13 September 2023
/
Published: 20 September 2023
(This article belongs to the Section Immunology)
Simple Summary
The hygiene hypothesis suggests that some infections may inhibit the development of allergic diseases, but the mechanism remains unclear. This research demonstrated the important role of cytokine-producing B cells in the infection-mediated modulation of allergic responses. Using chlamydia as a model pathogen, we showed that the adoptive transfer of B cells isolated from chlamydia-infected mice, unlike those from naïve mice, could effectively inhibit allergic airway eosinophilia and mucus overproduction, as well as Th2 cytokine responses. Intracellular cytokine analysis showed that B cells from chlamydia-infected mice produced higher levels of IFNγ than those from naïve mice. The inhibitory effect of the adoptively transferred B cells on allergic reactions was virtually abolished by the simultaneous blockade of IFNγ using a monoclonal antibody, which suggested that B cells modulated by chlamydial lung infection could have an inhibitory effect on airway allergic responses via the production of IFNγ. The results provide new insights into the targets related to the prevention and treatment of allergic diseases.
Abstract
The hygiene hypothesis suggests that some infections may inhibit the development of allergic diseases, but the mechanism remains unclear. Our previous study has shown that Chlamydia muridarum (Cm) lung infection can inhibit local eosinophilic inflammation induced by ovalbumin (OVA) through the modulation of dendritic cell (DC) and T cell responses in mice. In this study, we explored the role of B cells in the chlamydial-infection-mediated modulation of allergic responses. The results showed that adoptive transfer of B cells isolated from Cm-infected mice (Cm-B cells), unlike those from naïve mice (naïve B cells), could effectively inhibit allergic airway eosinophilia and mucus overproduction, as well as Th2 cytokine responses. In addition, total IgE/IgG1 and OVA-specific IgE/IgG1 antibodies in the serum were also decreased by the adoptive transfer of Cm-B cells. Intracellular cytokine analysis showed that B cells from Cm-infected mice produced higher levels of IFNγ than those from naïve mice. More interestingly, the inhibiting effect of adoptively transferred Cm-B cells on allergic reactions was virtually abolished by the simultaneous blockade of IFNγ using a monoclonal antibody. The results suggest that B cells modulated by chlamydial lung infection could play a regulatory role in OVA-induced acute allergic responses in the lung via the production of IFNγ. The results provide new insights into the targets related to the prevention and treatment of allergic diseases.
Keywords:
B cells; chlamydial infection; asthma; IFNγ
