The Immune Regulatory Functions in B Cells Are Restored by CpG to Reduce Experimental Food Allergy
Funding: This study was supported by research grants of the National Natural Science Foundation of China (32090052, 82002397), Natural Science Foundation of Hunan Province, (2021JJ40868, 2023JJ60339), Shenzhen Key Medical Discipline Construction Fund (SZXK062), Shenzhen science, technology, and innovation committee (KQTD20170331145453160). Thanks for the support of National Traditional Chinese Medicine Advantage Specialist (Surgery) Funding.
The first three authors share the first authorship.
ABSTRACT
Dysfunctional immune regulation contributes to the pathogenesis of food allergy (FA). The mechanism behind regulatory B-cell dysfunction is unclear. CpG has immune regulatory functions. The purpose of this study is to use CpG to recover the immune suppressive functions of B cells in mice with FA. An FA mouse model was created using ovalbumin as the specific antigen. Flow cytometry was used to isolate B cells from the intestinal tissues. The immune regulatory functions of B cells were assessed using immunological approaches. The results showed that the FA response was linked to low IL-10 levels in gut lavage fluids of FA mice. FA mouse intestinal B cells produced lower amounts of IL-10 as compared with B cells isolated from naïve control mice. Impaired immune suppressive functions were observed in B cells isolated from the FA mouse intestine. The inducibility of the Il10 expression in naïve B cells of the intestine of FA mice was defective. The induction of Il10 expression in FA B cells could be restored by CpG through regulating the methylation status of the Cmip promoter. CpG promoted the therapeutic efficacy of allergen specific immunotherapy by restoring the induction of IL-10+ B cells in the intestine. The expression of Il10 in B cells of the FA mouse intestine was impaired. Administration of CpG could restore the expression of Il10 in B cells in the intestine and promote immunotherapy for FA.
Conflicts of Interest
The authors declare no conflicts of interest.
Open Research
Data Availability Statement
All the data are included in this paper.
