Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/145608
Title: TACI constrains TH17 pathogenicity and protects against gut inflammation
Authors: Tan, Andy Hee-Meng
Tso, Gloria Hoi Wan
Zhang, Biyan
Teo, Pei-Yun
Ou, Xijun
Ng, Sze-Wai
Wong, Alex Xing Fah
Tan, Sean Jing Xiang
Sanny, Arleen
Kim, Susana Soo-Yeon
Lee, Alison P.
Xu, Shengli
Lam, Kong-Peng
Keywords: Science::Biological sciences
Issue Date: 2020
Source: Tan, A. H.-M., Tso, G. H. W., Zhang, B., Teo, P.-Y., Ou, X., Ng, S.-W., . . . Lam, K.-P. (2020). TACI constrains TH17 pathogenicity and protects against gut inflammation. iScience, 23(11), 101707-. doi:10.1016/j.isci.2020.101707
Journal: iScience
Abstract: TACI (transmembrane activator and calcium modulator and cyclophilin ligand interactor) plays critical roles in B cells by promoting immunoglobulin class switching and plasma cell survival. However, its expression and function in T cells remain controversial. We show here that TACI expression can be strongly induced in murine CD4+ T cells in vitro by cytokines responsible for TH17 but not TH1 or TH2 differentiation. Frequencies and numbers of TH17 cells were elevated in TACI−/− compared with wild-type mice as well as among TACI−/− versus wild-type CD4+ T cells in mixed bone marrow chimeras, arguing for a T cell-intrinsic effect in the contribution of TACI deficiency to TH17 cell accumulation. TACI−/− mice were more susceptible to severe colitis induced by dextran sodium sulfate or adoptive T cell transfer, suggesting that TACI negatively regulates TH17 function and limits intestinal inflammation in a cell-autonomous manner. Finally, transcriptomic and biochemical analyses revealed that TACI−/− CD4+ T cells exhibited enhanced activation of TH17-promoting transcription factors NFAT, IRF4, c-MAF, and JUNB. Taken together, these findings reveal an important role of TACI in constraining TH17 pathogenicity and protecting against gut disease.
URI: https://hdl.handle.net/10356/145608
ISSN: 2589-0042
DOI: 10.1016/j.isci.2020.101707
Rights: © 2020 The Author(s). This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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