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Maintaining NET balance

In cystic fibrosis, the rationale for antagonizing CXC chemokine receptor 2 has been to minimize the recruitment of immune cells to the inflamed lung by the receptor's chemokine ligands. Now, a team at the University of Tuebingen has shown that antagonists of the receptor also can stop the formation of neutrophil extracellular traps, which contribute to the buildup of DNA and protein that impairs lung functionin CF patients.1

The mechanistic link uncovered here could mean that inhibitors of CXC chemokine receptor 2 (CXCR2; IL8RB) also have therapeutic potential for other inflammatory diseases in which neutrophil extracellular traps (NETs) play a role, such as systemic lupus erythematosus (SLE), vasculitis

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