Atypical chemokine receptors—“chemokine PACMANs” as new therapeutic targets in glomerulonephritis

Abstract

Inflammatory cells are recruited to sites of inflammation by chemokines. Atypical chemokine receptors regulate chemokine gradients, thereby limiting inflammation. In this issue of Kidney International, atypical chemokine receptor 2 knockouts were described to be increasingly susceptible to immune complex-mediated glomerulonephritis. By degrading CCL2, atypical chemokine receptor 2 limited the recruitment of immune cells and myofibroblasts to the renal interstitial compartment. Therefore, not only inflammation, but also fibrosis, was effectively inhibited, making atypical chemokine receptor 2 an attractive therapeutic target in glomerulonephritis.