In human neutrophils, the expression of CCRL2 was increased by proinflammatory stimuli, such as LPS or TNF-α alone or in combination with IFN-γ or GM-CSF (Galligan et al., 2004) and in neutrophils isolated from inflamed joints of arthritis patients (Auer et al., 2007). Here, CCRL2 is linked to arthritic joint disease.