Fig. 2From: Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosisRole of different cells in the pathogenesis of MS and EAE. In the thymus, thymocyte precursor cells develop into γδT1, γδT17, nTregs and naïve CD4+ T cells. Upon neuroinflammation, γδT1 and γδT17 cells can cross the endothelial BBB and traffic into the central nervous system CNS, whereas naïve T cells migrate into the peripheral immune tissue. Naïve T cells connected with APCs (DCs and B cells), thereby differentiating into various effector T cells (iTregs, Tr1, Th17 and Th1). Th1, Th17, γδT1 and γδT17 cells secrete pro-inflammatory cytokines that trigger neuroinflammation and impair the myelin sheath and axons. Meanwhile, Tregs (Tr1, iTregs and nTregs) secrete anti-inflammatory cytokines and restrain immune responses mediated by T cells, B cells and DCs, thereby promoting tissue repair. Further, with the help of Tfh cells, naïve B cells differentiate into plasma cells, memory B cells and Bregs. While plasma cells damage the myelin sheath and axons on neurons via secreting antibodies, Bregs play a protective role via producing IL10, IL35 and TGF-β. Memory B cells and several activated B cells can produce a series of pathogenic cytokinesAbbreviations: MS: multiple sclerosis; EAE: experimental autoimmune encephalomyelitis; γδ: gamma delta; BBB: blood-brain barrier; CNS: central nervous system; APC: professional antigen presenting cells; DC: dendritic cell; iTreg: induced regulatory T cell; Tr1: type 1 Treg; Th: T helper; nTreg: natural regulatory T cell; Tfh: follicular helper T; Breg: regulatory B cell; IL: interleukin; IFN-γ: interferon-γ; TGF-β: transforming growth factor-β; TNF-α: tumor necrosis factor α; GM-CSF: granulocyte monocyte-colony stimulating factorBack to article page