Regulatory B cells in infection, inflammation, and autoimmunity

Abstract

Regulatory B (Breg) cells are characterized by differential expression of CD5 and CD1d in mouse and CD24 and CD38 in human immune systems. The Breg family also includes LAG-3⁺CD138^hi plasma cells, CD1d CD5 CD21 CD23 cells, Tim1, PD-L1, PD-L2, CD200- expressing B cells, and CD39^hiKi67⁺ cells originating from the transitional, marginal zone or germinal centre of the spleen. Breg cells produce IL10 and IL35 and to cause immunosuppression. These cells respond to TLR2, TLR4, and TLR9 agonists, CD40 ligands, IL12p35 and heat shock proteins. Emerging evidence suggests that TLR signalling component Myd88 impacts the modulation of Breg cell responses and the host's susceptibility to infection. Breg cells are found to reduce relapsing-remitting experimental autoimmune encephalomyelitis. However, the Breg-mediated mechanism used to control T cell-mediated immune responses is still unclear. Here, we review the existing literature to find gaps in the current knowledge and to build a pathway to further research.

Keywords: Autoimmunity; B cells; Breg cells; EAE; Immunosuppression; Inflammation; Tolerance; Toll-like receptor.