한빛사 논문
Seung-Ah Yoo1,2,9, Mingyo Kim3,4,9, Min-Cheol Kang5,9, Jin-Sun Kong1,2, Ki-Myo Kim1,2, Saseong Lee1,2, Bong-Ki Hong1,2, Gi Heon Jeong1,2, Jinhee Lee5, Min-Gyeong Shin6, Yeon-Gu Kim6, Ivana Apicella7, Valeria Cicatiello7, Sandro De Falco7, Chong-Hyeon Yoon1,8, Chul-Soo Cho1,8, Zae Young Ryoo5*, Seung-Hyo Lee3* and Wan-Uk Kim1,2,8*
1 Center for Integrative Rheumatoid Transcriptomics and Dynamics, The Catholic University of Korea, Seoul, Korea. 2 Department of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, Korea. 3 Graduate School of Medical Science and Engineering, BioMedical Research Center, KAIST Institute for the BioCentury, Korea Advanced Institute of Science and Technology, Daejeon, Korea. 4 Division of Rheumatology, Department of Internal Medicine, Gyeongsang National University Hospital, Jinju, Korea. 5 School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, Korea. 6 Biotherapeutics Translational Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea. 7 Istituto di Genetica e Biofisica Adriano Buzzati-Traverso, National Research Council, Napoli, Italy. 8 Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea. 9 These author contributed equally: Seung-Ah Yoo, Mingyo Kim and Min-Cheol Kang.
*Correspondence to Zae Young Ryoo or Seung-Hyo Lee or Wan-Uk Kim
Abstract
Helper T cells actively communicate with adjacent cells by secreting soluble mediators, yet crosstalk between helper T cells and endothelial cells remains poorly understood. Here we found that placental growth factor (PlGF), a homolog of the vascular endothelial growth factor that enhances an angiogenic switch in disease, was selectively secreted by the TH17 subset of helper T cells and promoted angiogenesis. Interestingly, the ‘angio-lymphokine’ PlGF, in turn, specifically induced the differentiation of pathogenic TH17 cells by activating the transcription factor STAT3 via binding to its receptors and replaced the activity of interleukin-6 in the production of interleukin-17, whereas it suppressed the generation of regulatory T cells. Moreover, T cell-derived PlGF was required for the progression of autoimmune diseases associated with TH17 differentiation, including experimental autoimmune encephalomyelitis and collagen-induced arthritis, in mice. Collectively, our findings provide insights into the PlGF-dictated links among angiogenesis, TH17 cell development and autoimmunity.
논문정보
관련 링크
연구자 ID
관련분야 연구자보기
관련분야 논문보기