| First Author | Christensen AD | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 5 | Pages | 1235-45 |
| PubMed ID | 26848119 | Mgi Jnum | J:246718 |
| Mgi Id | MGI:5922348 | Doi | 10.1002/eji.201546185 |
| Citation | Christensen AD, et al. (2016) Granulocyte colony-stimulating factor (G-CSF) plays an important role in immune complex-mediated arthritis. Eur J Immunol 46(5):1235-45 |
| abstractText | Neutrophils are an abundant cell type in many chronic inflammatory diseases such as rheumatoid arthritis (RA); however, their contribution to the pathology of RA has not been widely studied. A key cytokine involved in neutrophil development and function is granulocyte-colony stimulating factor (G-CSF). In this study we used the K/BxN serum-transfer arthritis (STA) model, mimicking the effector phase of RA, to investigate the importance of G-CSF in arthritis development and its relation to neutrophils. Here, we show for the first time in this model that G-CSF levels are increased both in the serum and in inflamed paws of arthritic mice and importantly that G-CSF blockade leads to a profound reduction in arthritis severity, as well as reduced numbers of neutrophils in blood. Moreover, CXCL1 and CXCL2 levels in the arthritic joints were also lowered. Our data demonstrate that G-CSF is a pivotal driver of the disease progression in the K/BxN STA model and possibly acts in part by regulating neutrophil numbers in the circulation. Therefore, our findings suggest that G-CSF might be a suitable target in RA, and perhaps in other immune complex-driven pathologies. |
