Identification of Acvr2a as a Th17 Cell-Specific Gene Induced during Th17 Differentiation

• Published in: Bioscience, biotechnology, and biochemistry Vol. 75; no. 11; pp. 2138 - 2141
• Main Authors: IHN, Hyun-ju, KIM, Dong Hyeok, OH, Sang-Seok, MOON, Chaerin, CHUNG, Jin Woong, SONG, Hyunkeun, KIM, Kwang Dong
• Format: Journal Article
• Language: English
• Published: Tokyo Japan Society for Bioscience, Biotechnology, and Agrochemistry 2011; Japan Society for Bioscience Biotechnology and Agrochemistry; Oxford University Press
• Subjects: Activin Receptors, Type II - genetics; Activin Receptors, Type II - immunology; Activin Receptors, Type II - metabolism; Acvr2a; all trans retinoic acid (ATRA); Animals; Biological and medical sciences; Cell Differentiation; Cell Lineage; Female; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation; helper type 17 T cell (Th17); IL-6; Interleukin-6 - metabolism; Mice; Mice, Inbred C57BL; T-Lymphocytes, Regulatory - immunology; TGF-β; Th1 Cells - metabolism; Th17 Cells - immunology; Th17 Cells - metabolism; Th2 Cells - metabolism; Transforming Growth Factor beta - metabolism; Tretinoin - pharmacology; Interleukin 6; helper type 17 T cell (Th17); Gene; all trans retinoic acid (ATRA); Cytokine; Acvr2a; TGF-β; Identification; Differentiation; IL-6; Tretinoin
• ISSN: 0916-8451; 1347-6947; 1347-6947
• DOI: 10.1271/bbb.110436

IL-17-producing T lymphocytes have been found to comprise a distinct lineage of T helper cells (Th17 cells) that are major causes of autoimmune diseases such as EAE, RA, and IBD. In this study, we found that activin receptor type-2A (Acvr2a) is a gene induced during the differentiation of this effector cell lineage as compared with naïve T cells. The transcript of Acvr2a was not induced in Th1 and Th2 cells, and both TGF-β and IL-6 were required for the induction of Acvr2a. When the differentiation of Th17 cells was inhibited by all tarans retinoic acid (ATRA) which induces regulatory T cell (Treg) differentiation under Th17 differentiation conditions, expression of Acvr2a was also inhibited. Hence we propose that Acvr2a is a Th17 specific gene making Th17 cells distinct from other helper T cells, Th1, Th2, and Treg.