In contrast, neither an anti-CSF-1R mAb nor an anti-CSF-1 mAb reduced arthritis, suggesting lack of involvement of CSF-1 and IL-34, and possibly reflecting the high neutrophil component and the relatively acute nature of the model compared with other more chronic and more macrophage-dependent arthritis models where such blockade was effective [45–47]. Here, CSF1 is linked to arthritic joint disease.