Plasma Cells: From Cytokine Production to Regulation in Experimental Autoimmune Encephalomyelitis

Abstract

B cells are a critical arm of the adaptive immune system. After encounter with antigen, B cells are activated and differentiate into plasmablasts (PBs) and plasma cells (PCs). Although their frequency is low, PB/PCs can be found in all lymphoid organs including peripheral lymph nodes and spleen. Upon immunization, depending on the location of where B cells encounter their antigen, PB/PCs subsequently home to and accumuate in the bone marrow and the intestine where they can survive as long-lived plasma cells for years, continually producing antibody. Recent evidence has shown that, in addition to producing antibodies, PB/PCs can also produce cytokines such as IL-17, IL-10, and IL-35. In addition, PB/PCs that produce IL-10 have been shown to play a regulatory role during experimental autoimmune encephalomyelitis, an animal model of neuroinflammation. The purpose of this review is to describe the phenotype and function of regulatory PB/PCs in the context of experimental autoimmune encephalomyelitis and in patients with multiple sclerosis.

Keywords: experimental autoimmune encephalomyelitis; multiple sclerosis; plasma cells; regulatory B cells.