Abstract
Regulatory B cells (Bregs) have an anti-inflammatory role and can suppress autoimmunity, by employing both cytokine secretion and cell-contact mediated mechanisms. Numerous Breg subsets have been described and have overlapping phenotypes in terms of their immune expression markers or cytokine production. A hallmark feature of Bregs is the secretion of IL-10, although IL-35 and TGFβ−producing B cells have also been identified. To date, few reports have identified an impaired frequency or function of Bregs in individuals with type 1 diabetes; thus our understanding of the role played by these Breg subsets in the pathogenesis of this condition is limited. In this review we will focus on how regulatory B cells are altered in the development of type 1 diabetes, highlighting both frequency and function and discuss both human and animal studies.
Highlights
It is well-established that regulatory B cells (Bregs) can dampen immune responses and play a role in maintaining immune tolerance
Studies of other autoimmune diseases have highlighted the essential role for regulatory B cells [8] and this has been reflected in type 1 diabetes, comparatively with fewer studies
In NOD mice with established diabetes, that CD40-ligation on B cells, followed by co-culture with DCs, the ability to reduce DC activation was decreased and resulted in a contact-dependent increase in IFNg secretion, compared to NOD mice naturally-protected from autoimmune diabetes [60]
Summary
It is well-established that regulatory B cells (Bregs) can dampen immune responses and play a role in maintaining immune tolerance. In type 1 diabetes B cells are typically understood to play a pathogenic role in disease, likely through the production of inflammatory cytokines and presentation of autoantigens to T cells [6]. This has been emphasized by the use of Rituximab in clinical trials and the observed temporary delay in the loss of C-peptide [7]. This review will focus on the emerging literature on Bregs and discuss their role in type 1 diabetes
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