Granulocyte colony‐stimulating factor (G‐CSF) plays an important role in immune complex‐mediated arthritis

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.