m 6 A demethylase ALKBH5 controls CD4 + T cell pathogenicity and promotes autoimmunity

Author:

Zhou Jing123ORCID,Zhang Xingli12ORCID,Hu Jiajia4ORCID,Qu Rihao56ORCID,Yu Zhibin12ORCID,Xu Hao3,Chen Huifang12,Yan Lichong3,Ding Chenbo123ORCID,Zou Qiang1ORCID,Ye Youqiong1ORCID,Wang Zhengting7ORCID,Flavell Richard A.38ORCID,Li Hua-Bing123ORCID

Affiliation:

1. Shanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

2. Shanghai Jiao Tong University School of Medicine–Yale Institute for Immune Metabolism, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

3. Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520-8055, USA.

4. Department of Nuclear Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

5. Program of Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA.

6. Department of Pathology, Yale School of Medicine, New Haven, CT 06510, USA.

7. Department of Gastroenterology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

8. Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520-8055, USA.

Abstract

ALKBH5 maintains CD4 + T cell pathogenicity during autoimmune disease via regulating IFN-γ and CXCL2.

Funder

Howard Hughes Medical Institute

Shanghai Science and Technology Development Fund

National Natural Science Foundation of China

Shanghai Super Postdoctoral Program

China Postdoctoral Science Foundation

Postdoctoral Innovation Talent Support Program

Shanghai Jiao Tong University School of Medicine

Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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