Asset Details
Do you wish to reserve the book?
A critical role for Th17 cell-derived TGF-β1 in regulating the stability and pathogenicity of autoimmune Th17 cells
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
A critical role for Th17 cell-derived TGF-β1 in regulating the stability and pathogenicity of autoimmune Th17 cells
Do you wish to request the book?
A critical role for Th17 cell-derived TGF-β1 in regulating the stability and pathogenicity of autoimmune Th17 cells
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
A critical role for Th17 cell-derived TGF-β1 in regulating the stability and pathogenicity of autoimmune Th17 cells
2021
Overview
Pathogenic conversion of Th17 cells into multifunctional helper T cells or Th1 cells contributes to the pathogenesis of autoimmune diseases; however, the mechanism regulating the plasticity of Th17 cells remains unclear. Here, we found that Th17 cells expressed latent TGF-β1 in a manner dependent on autocrine TGF-β1. By employing IL-17-producing cell-specific
Tgfb1
conditional knockout and fate-mapping systems, we demonstrated that TGF-β1-deficient Th17 cells are relatively susceptible to becoming IFN-γ producers through IL-12Rβ2 and IL-27Rα upregulation. TGF-β1-deficient Th17 cells exacerbated tissue inflammation compared to TGF-β1-sufficient Th17 cells in adoptive transfer models of experimental autoimmune encephalomyelitis and colitis. Thus, TGF-β1 production by Th17 cells provides an essential autocrine signal for maintaining the stability and regulating the pathogenicity of Th17 cells in vivo.
Autoimmune disease: Transforming growth factor keeps subset of T cells in check
A protein secreted by pro-inflammatory immune cells acts on the same secreting cells to prevent their conversion into pathogenic drivers of autoimmune disease. A team in South Korea led by Byung-Seok Kim from Incheon National University and Yeonseok Chung from Seoul National University showed that T helper 17 (Th17) cells, a subset of T helper cells defined by their production of a signaling molecule known as interleukin 17, express a protein called transforming growth factor-β1 (TGF-β1) that maintains the stability of Th17 in a self-regulating manner. Without the ability to produce TGF-β1, the cells tend to convert into a form that fuel disease-associated inflammation in mouse models of multiple sclerosis and colitis. Therapeutic blockade of this conversion process could help treat diseases linked to Th17 cell–mediated autoimmunity.
Publisher
Nature Publishing Group UK,Springer Nature B.V,생화학분자생물학회
Subject
/ 13/106
/ 13/31
/ 38/90
/ 64/60
/ 96/21
/ Animals
/ Biomedical and Life Sciences
/ Colitis
/ Disease
/ Encephalomyelitis, Autoimmune, Experimental - etiology
/ Encephalomyelitis, Autoimmune, Experimental - metabolism
/ Encephalomyelitis, Autoimmune, Experimental - pathology
/ Experimental allergic encephalomyelitis
/ Mice
/ Receptors, Interleukin - genetics
/ Receptors, Interleukin - metabolism
/ Receptors, Interleukin-12 - genetics
/ Receptors, Interleukin-12 - metabolism
/ T-Lymphocyte Subsets - immunology
/ T-Lymphocyte Subsets - metabolism
/ Transforming Growth Factor beta1 - genetics
/ Transforming Growth Factor beta1 - metabolism
/ Transforming growth factor-b1
/ 생화학
