7/29/2023 0 Comments Antibody production cellsHowever, TGF-β1, when present with inflammatory cytokines, may promote inflammation by promoting the differentiation of Th17 cells. TGF-β1 also inhibits excessive immune response by promoting induction and maintenance of Foxp3 + regulatory T cells (Treg cells), and TGF-β1 contributes to the immunosuppressive function of Foxp3 + Treg cells. TGF-β1 inhibits proliferation of T cells, as well as T cell differentiation into Th1 cells and Th2 cells. Of the three isoforms of TGF-β, TGF-β1 had mainly received attention in immunology until recently and is generally known as an inhibitory cytokine, although it exhibits immunostimulatory functions in certain conditions. For example, TGF-β1 promotes fibrosis during wound healing, but TGF-β3 has anti-fibrotic effects. In certain contexts, different isoforms exhibit opposing effects. TGF-β2 knockout mice exhibit various congenital abnormalities involving the cardiovascular, pulmonary, skeletal, and urogenital systems, and TGF-β3 knockout mice exhibit cleft palate and delayed lung development. TGF-β1 knock out mice develop autoinflammatory disease characterized by inflammation in various organs and production of autoantibodies. Each isoform is thought to have different biological roles in vivo as the expression of the three isoforms differ in their pattern of expression and knock out mice of different isoforms exhibit different phenotypes. There are three isoforms of TGF-β in mammals. Transforming growth factor-beta (TGF-β) is a pleotropic cytokine involved in various biological processes. This does not alter our adherence to PLOS ONE policies on sharing data and materials. The other authors declare no competing financial interests. KF received financial support or fees from Astellas, BMS, Daiichi-Sankyo, MitsubishiTanabe, Pfizer, Santen, Takeda, Chugai, Eisai, Taisho Toyama and UCB,and Janssen. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: KY received financial support or fees from AbbVie, Astellas, BMS, Daiichi-Sankyo, MitsubishiTanabe, Pfizer, Sanofi, Santen, Takeda, Teijin, Boehringer Ingelheim, Chugai, Eisai, Ono, Taisho Toyama, UCB, ImmunoFuture, Asahi Kasei, and Janssen. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper and its Supporting Information file.įunding: This work was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology, KAKENHI Grant-in-Aid for Scientific Research (S) (23229007) (received by KY and KF) and KAKENHI Grant-in-Aid for Young Scientists (B) (15K19566) (received by SS) from Japan Society for the Promotion of Science. Received: AugAccepted: DecemPublished: January 4, 2017Ĭopyright: © 2017 Tsuchida et al. PLoS ONE 12(1):Įditor: Yeonseok Chung, Seoul National University College of Pharmacy, REPUBLIC OF KOREA (2017) TGF-β3 Inhibits Antibody Production by Human B Cells. Our results suggest that TGF-β3 modifying therapy might be therapeutic in autoimmune diseases with B cell dysregulation in humans.Ĭitation: Tsuchida Y, Sumitomo S, Ishigaki K, Suzuki A, Kochi Y, Tsuchiya H, et al. TGF-β1 and β3 also inhibited B cell receptor signaling. TGF-β1 and TGF-β3 inhibited some of the key molecules of the cell cycle, as well as transcription factors important in B cell differentiation into antibody secreting cells such as IRF4, Blimp-1, and XBP1. Although the suppression of human B cells by TGF-β1 has long been recognized, the precise mechanism for the suppression of B cell function by TGF-β1 remains elusive therefore, we examined the effect of TGF-β1 and β3 on pathways important in B cell activation and differentiation. ![]() ![]() TGF-β3 suppressed B cell survival, proliferation, differentiation into plasmablasts, and antibody secretion. The effect of TGF-β3 on human B cells has not been reported, and we herein examined the effect of TGF-β3 on human B cells. Murine CD4 +CD25 -LAG3 + regulatory T cells suppress B cell function through the production of TGF-β3, and it has been reported that TGF-β3 is therapeutic in a mouse model of systemic lupus erythematosus. Recently, it has been suggested that TGF-β3 may play an important role in the regulation of immune system in mice. Of the three isoforms of TGF-β, TGF-β1 has long been recognized as an important inhibitory cytokine in the immune system and has been reported to inhibit B cell function in both mice and humans. TGF-β is a pleotropic cytokine involved in various biological processes.
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