Regulatory B cells in parasitic infections: roles and therapeutic potential

Abstract

Parasitic infection is a complex process involving interactions among various immune cells. Regulatory B cells (Breg cells), a subset of B lymphocytes with immunosuppressive functions, play a role in modulating immune responses during infection to prevent excessive immune activation. This article reviews the origin, phenotype, and immunoregulatory mechanisms of Breg cells. We summarize the immunomodulatory roles of Breg cells in various parasitic infections. We also discuss the potential applications of activating Breg cells through parasitic infections and their derived molecules in the treatment of certain allergic, autoimmune, and inflammatory diseases. The aim is to provide new perspectives for the future treatment of parasitic diseases and other related conditions.

Keywords: Allergy; Immunoregulation; Inflammation; Parasitic infections; Regulatory B cells.

Fig. 1

Proposed development and differentiation pathways of Breg cells. In response to the influence of Toll-like receptor (TLR) ligands, CD40, and various cytokines, immature B cells are capable of differentiating into several forms, including B10 cells, T2-MZP cells, and mature B cells. These cell forms serve as precursors to regulatory B cells. Furthermore, both B10 and T2-MZP cells have the capacity to differentiate into mature B cells. Furthermore, from these mature B cells, plasmablasts that are capable of secreting cytokines such as IL-10, IL-35, and TGF-β can develop. Finally, regulatory B cells have the potential to differentiate into conventional plasma cells, which are responsible for antibody production

Fig. 2

The impact of Breg cells on other immune cells. Regulatory B cells are pivotal in sustaining immune system balance and tolerance through multiple mechanisms. They efficiently curb the growth, differentiation, and functionality of CD4⁺ and CD8⁺ T cells through the release of anti-inflammatory cytokines like interleukin-10 (IL-10), IL-35, and transforming growth factor-beta (TGF-β). Additionally, Bregs influence T cell activities by reducing pro-inflammatory factor production in dendritic cells, decreasing the activities of Th1, Th17, and CD8⁺ T cells, and fostering the transformation of CD4⁺ T cells into regulatory T cells (Tregs) and IL-10-producing Type 1 regulatory T cells (Tr1). Moreover, they suppress tumor necrosis factor-alpha (TNF-α) production in monocytes, curtail interferon-alpha (IFN-α) secretion by plasmacytoid dendritic cells (PDCs) and IL-12-dependent dendritic cells, promoting Th2-type responses