Immunometabolism in the development of rheumatoid arthritis
Open accessAbstract
In rheumatoid arthritis (RA), breakdown of self‐tolerance and onset of clinical disease are separated in time and space, supporting a multi‐hit model in which emergence of autoreactive T cells is a pinnacle pathogenic event. Determining factors in T cell differentiation and survival include antigen recognition, but also the metabolic machinery that provides energy and biosynthetic molecules for cell building. Studies in patients with RA have yielded a disease‐specific metabolic signature, which enables naive CD4 T cells to differentiate into pro‐inflammatory helper T cells that are prone to invade into tissue and elicit inflammation through immunogenic cell death. A typifying property of RA CD4 T cells is the shunting of glucose away from glycolytic breakdown and mitochondrial processing toward the pentose phosphate pathway, favoring anabolic over catabolic reactions. Key defects have been localized to the mitochondria and the lysosome; including instability of mitochondrial DNA due to the lack of the DNA repair nuclease MRE11A and inefficient lysosomal tethering of AMPK due to deficiency of N‐myristoyltransferase 1 (NMT1). The molecular taxonomy of the metabolically reprogrammed RA T cells includes glycolytic enzymes (glucose‐6‐phosphate dehydrogenase, phosphofructokinase), DNA repair molecules (MRE11A, ATM), regulators of protein trafficking (NMT1), and the membrane adapter protein TSK5. As the mechanisms determining abnormal T cell behavior in RA are unraveled, opportunities will emerge to interject autoimmune T cells by targeting their metabolic checkpoints.
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The balance between glycolysis and oxidative phosphorylation not only defines ATP yield but might also affect oxidation levels and consumption of metabolites such as glucose and fatty acids.
“The balance between glycolysis and oxidative phosphorylation in providing energy for the cell not only defines the yield of ATP production but might also affect the levels of oxidation (for example, through the production of mtROS) and the consumption of metabolites (such as glucose and fatty acids)273,274.”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [274]
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- Authors
- Weyand, C. M., & Goronzy, J. J.
- Affiliations
- VA Palo Alto Health Care System (US)
- Corresponding author
- Weyand, Cornelia M.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2020-01-27
- Volume
- 294
- Issue
- 1
- Pages
- 177-187
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- PMC
- PMC7047523
- OpenAlex
- W3000874222
- Cited by
- 193
- References
- 87
- Citations by year
- 2026: 31 · 2025: 40 · 2024: 30 · 2023: 35 · 2022: 24 · 2021: 16 · 2020: 15
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01AI108891, R01AG045779, U19AI057266, R01AI129191, R01AR042527, R01HL117913, R01AI108906, P01HL129941)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- rheumatoid arthritis, immunometabolism, CD4+ T cells, T cell differentiation, pentose phosphate pathway, mitochondrial DNA repair, MRE11A, NMT1, AMPK, lysosomes, glycolysis, autoreactive T cells, immunogenic cell death, metabolic reprogramming, metabolic checkpoint
- MeSH terms
- Animals, Arthritis, Rheumatoid, DNA Damage, DNA Repair, Glycolysis, Humans, Macrophages, Mitochondria, CD4-Positive T-Lymphocytes, Autoimmunity, Protein Transport
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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