| First Author | Lin T | Year | 2020 |
| Journal | Viruses | Volume | 12 |
| Issue | 11 | PubMed ID | 33147869 |
| Mgi Jnum | J:303287 | Mgi Id | MGI:6513643 |
| Doi | 10.3390/v12111252 | Citation | Lin T, et al. (2020) CXCL10 Signaling Contributes to the Pathogenesis of Arthritogenic Alphaviruses. Viruses 12(11) |
| abstractText | Emerging and re-emerging arthritogenic alphaviruses, such as Chikungunya virus (CHIKV) and O'nyong nyong virus, cause acute and chronic crippling arthralgia associated with inflammatory immune responses. Approximately 50% of CHIKV-infected patients suffer from rheumatic manifestations that last 6 months to years. However, the physiological functions of individual immune signaling pathways in the pathogenesis of alphaviral arthritis remain poorly understood. Here, we report that a deficiency in CXCL10, which is a chemoattractant for monocytes/macrophages/T cells, led to the same viremia as wild-type animals, but fewer immune infiltrates and lower viral loads in footpads at the peak of arthritic disease (6-8 days post infection). Macrophages constituted the largest immune cell population in footpads following infection, and were significantly reduced in Cxcl10(-/-) mice. The viral RNA loads in neutrophils and macrophages were reduced in Cxcl10(-/-) compared to wild-type mice. In summary, our results demonstrate that CXCL10 signaling promotes the pathogenesis of alphaviral disease and suggest that CXCL10 may be a therapeutic target for mitigating alphaviral arthritis. |
