<scp>ADAM9</scp> Promotes Glycolysis in Th17 Cells and Autoimmunity Through Activation of <scp>IGF</scp> ‐1 Signaling
By cleaving IGFBP4, ADAM9 releases IGF-1, which in turn upregulates GLUT1 expression and promotes glycolysis in Th17 cells. These findings suggest that targeting ADAM9 or blocking IGF-1 should provide a therapeutic strategy for autoimmune diseases.
Authors
- Theodoros Vichos (ORCID: https://orcid.org/0009-0002-7237-1954)
- George C. Tsokos (ORCID: https://orcid.org/0000-0001-9589-2360)
- Michihito Kono (ORCID: https://orcid.org/0000-0002-7663-534X)
- Masataka Umeda (ORCID: https://orcid.org/0000-0002-6647-7130)
- Maria Tsokos (ORCID: https://orcid.org/0000-0001-8072-1358)
- Kohei Karino (ORCID: https://orcid.org/0000-0001-5319-3174)
- Wenliang Pan (ORCID: https://orcid.org/0009-0003-5965-2126)
Institutions
- Beth Israel Deaconess Medical Center (US)
- Harvard University (US)
- Hokkaido University (JP)
Publication Details
- Journal
- Arthritis & Rheumatology
- Published
- 2025-07-21
- DOI
- https://doi.org/10.1002/art.43313
- Citations
- 3
- Primary Topic
- Cytokine Signaling Pathways and Interactions
- Type
- article
- Field-Weighted Citation Impact
- 3.14