| First Author | Koenders MI | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 10 | Pages | 6262-9 |
| PubMed ID | 16670337 | Mgi Jnum | J:131778 |
| Mgi Id | MGI:3774462 | Doi | 10.4049/jimmunol.176.10.6262 |
| Citation | Koenders MI, et al. (2006) Interleukin-17 acts independently of TNF-alpha under arthritic conditions. J Immunol 176(10):6262-9 |
| abstractText | The proinflammatory T cell cytokine IL-17 is a potent inducer of other cytokines such as IL-1 and TNF-alpha. The contribution of TNF in IL-17-induced joint inflammation is unclear. In this work we demonstrate using TNF-alpha-deficient mice that TNF-alpha is required in IL-17-induced joint pathology under naive conditions in vivo. However, overexpression of IL-17 aggravated K/BxN serum transfer arthritis to a similar degree in TNF-alpha-deficient mice and their wild-type counterparts, indicating that the TNF dependency of IL-17-induced pathology is lost under arthritic conditions. Also, during the course of the streptococcal cell wall-induced arthritis model, IL-17 was able to enhance inflammation and cartilage damage in the absence of TNF. Additional blocking of IL-1 during IL-17-enhanced streptococcal cell wall-induced arthritis did not reduce joint pathology in TNF-deficient mice, indicating that IL-1 is not responsible for this loss of TNF dependency. These data provide further understanding of the cytokine interplay during inflammation and demonstrate that, despite a strong TNF dependency under naive conditions, IL-17 acts independently of TNF under arthritic conditions. |
