| First Author | Li Y | Year | 2019 |
| Journal | Cell Rep | Volume | 27 |
| Issue | 10 | Pages | 2809-2816.e3 |
| PubMed ID | 31167128 | Mgi Jnum | J:280653 |
| Mgi Id | MGI:6368953 | Doi | 10.1016/j.celrep.2019.05.032 |
| Citation | Li Y, et al. (2019) Fat-Produced Adipsin Regulates Inflammatory Arthritis. Cell Rep 27(10):2809-2816.e3 |
| abstractText | We explored the relationship of obesity and inflammatory arthritis (IA) by selectively expressing diphtheria toxin in adipose tissue yielding "fat-free" (FF) mice completely lacking white and brown fat. FF mice exhibit systemic neutrophilia and elevated serum acute phase proteins suggesting a predisposition to severe IA. Surprisingly, FF mice are resistant to K/BxN serum-induced IA and attendant bone destruction. Despite robust systemic basal neutrophilia, neutrophil infiltration into joints of FF mice does not occur when challenged with K/BxN serum. Absence of adiponectin, leptin, or both has no effect on joint disease, but deletion of the adipokine adipsin (complement factor D) completely prevents serum-induced IA. Confirming that fat-expressed adipsin modulates the disorder, transplantation of wild-type (WT) adipose tissue into FF mice restores susceptibility to IA, whereas recipients of adipsin-deficient fat remain resistant. Thus, adipose tissue regulates development of IA through a pathway in which adipocytes modify neutrophil responses in distant tissues by producing adipsin. |
