Abstract
Transitional B cells (TrB cells) represent a crucial link between immature B cells in the bone marrow and mature peripheral B cells. Although TrB cells represent one of the regulatory B cell subpopulations in healthy individuals, the frequency of CD24hiCD38hi TrB cells in circulation may be altered in individuals with autoimmune diseases, such as multiple sclerosis, neuromyelitisoptica spectrum disorders, systemic lupus erythematosus, Sjögren’s syndrome, rheumatoid arthritis, systemic sclerosis, and juvenile dermatomyositis. Although TrB cells play regulatory roles under inflammatory conditions, consequences of their functional impairment vary across autoimmune diseases. Since the origin, development, and function of TrB cells, especially in humans, remain unclear and controversial, this review aimed to discuss the characteristics of TrB cells at steady state and explore their role in various immune diseases, including autoimmune rheumatic diseases and neuroimmunological diseases.
Highlights
B cells are centrally involved in the pathogenesis of autoimmunity, exerting diverse effects such as contributing to T cell activation through antibody production and antigen presentation
The findings revealed IL-4 to contribute to TrB cell differentiation and maturation both in mice and humans
systemic lupus erythematosus (SLE) plasma with IFN-α efficiently induces IL-6 expression in TrB cells, indicating IFN-α to possibly play an important role in stimulating TrB cells to produce IL-6 [68]. These findings indicate that the participation of TrB cells in pathogenesis of autoimmune rheumatic diseases (AIRDs), and reveal that impairment of their immune-regulatory functions may reflect their inability to prevent the processes underlying autoreactive responses and inflammation
Summary
B cells are centrally involved in the pathogenesis of autoimmunity, exerting diverse effects such as contributing to T cell activation through antibody production and antigen presentation. Transitional B cells (TrB cells) are bone marrowderived, immature B cells, which are considered to be precursors of mature B cells [3, 4]. Deletion of TrB cells resulted in a lack of mature B cell compartments during T. brucei infection, preventing the host’s ability of sustaining antibody responses against recurring parasitemic waves [19]. Since they are associated with several inflammatory diseases and are found in circulation as well as tissues of healthy individuals, TrB cells are thought to perform distinct functions in immune-defense mechanisms
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