Cytoplasmic zinc promotes IL-1β production by monocytes and macrophages through mTORC1-induced glycolysis in rheumatoid arthritis

Author:

Kim Bonah1ORCID,Kim Hee Young123,Yoon Bo Ruem2,Yeo Jina4ORCID,In Jung Ji4ORCID,Yu Kyung-Sang5ORCID,Kim Hyeon Chang6ORCID,Yoo Su-Jin7ORCID,Park Jin Kyun4ORCID,Kang Seong Wook7ORCID,Lee Won-Woo128ORCID

Affiliation:

1. Laboratory of Autoimmunity and Inflammation (LAI), Department of Biomedical Sciences, and BK21Plus Biomedical Science Project, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.

2. Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.

3. Institute of Infectious Diseases, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.

4. Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.

5. Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine and Hospital, Seoul 03080, Republic of Korea.

6. Department of Preventive Medicine, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.

7. Department of Internal Medicine, Chungnam National University School of Medicine, 282 Munhwa-ro, Jung-gu, Daejeon 35015, Republic of Korea.

8. Cancer Research Institute, Ischemic/Hypoxic Disease Institute, and Institute of Infectious Diseases, Seoul National University College of Medicine, Seoul National University Hospital Biomedical Research Institute, Seoul 03080, Republic of Korea.

Abstract

Zinc metabolically reprograms monocytes and macrophages to promote inflammation in rheumatoid arthritis.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

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