| First Author | Ren T | Year | 2024 |
| Journal | Sci Adv | Volume | 10 |
| Issue | 22 | Pages | eadk5011 |
| PubMed ID | 38809975 | Mgi Jnum | J:351315 |
| Mgi Id | MGI:7666165 | Doi | 10.1126/sciadv.adk5011 |
| Citation | Ren T, et al. (2024) Exercise activates interferon response of the liver via Gpld1 to enhance antiviral innate immunity. Sci Adv 10(22):eadk5011 |
| abstractText | Healthy behavioral patterns could modulate organ functions to enhance the body's immunity. However, how exercise regulates antiviral innate immunity remains elusive. Here, we found that exercise promotes type I interferon (IFN-I) production in the liver and enhances IFN-I immune activity of the body. Despite the possibility that many exercise-induced factors could affect IFN-I production, we identified Gpld1 as a crucial molecule, and the liver as the major organ to promote IFN-I production after exercise. Exercise largely loses the efficiency to induce IFN-I in Gpld1(-/-) mice. Further studies demonstrated that exercise-produced 3-hydroxybutanoic acid (3-HB) critically induces Gpld1 expression in the liver. Gpld1 blocks the PP2A-IRF3 interaction, thus enhancing IRF3 activation and IFN-I production, and eventually improving the body's antiviral ability. This study reveals that exercise improves antiviral innate immunity by linking the liver metabolism to systemic IFN-I activity and uncovers an unknown function of liver cells in innate immunity. |
