title: Professional and part-time chemokine decoys in the resolution of inflammation.
abstract: Inflammation is essential for protection from infection and for the repair of damaged tissue. Much is now known about how inflammation is induced and maintained, but the processes underlying the resolution of inflammation are often overlooked. However, resolution is an essential component of all successful inflammatory responses because it ensures the restoration of tissue homeostasis and prevents immunopathology of the type seen in chronic inflammatory diseases and autoimmunity. Small secreted proteins called chemokines, acting through chemokine receptors, are known to be critical regulators of leukocyte recruitment and function during the initiation and maintenance of inflammation. Thus, their efficient removal would seem to be a prerequisite for successful resolution. In recent years, it has emerged that specialized chemokine "decoy" receptors exist that actively participate in this process. Moreover, other chemokine receptors have been proposed to lead a double life and perform opposing roles during inflammation: leukocyte recruitment (by signaling) and resolution (by chemokine sequestration). A recent study provides further support for this theory by showing that apoptotic inflammatory leukocytes increase the number of surface chemokine receptors and that these receptors can remove chemokines from inflamed tissue. Leukocyte apoptosis is already known to aid resolution, not just because it eliminates leukocytes from inflamed tissues, but also because their consumption by macrophages leads to the production of anti-inflammatory cytokines. The new work indicates that chemokine sequestration may be another mechanism exploited by dying cells to assist in the resolution of inflammation.
authors.affiliation: Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, Glasgow University, Glasgow, Scotland, UK.
authors.forename: Chris
authors.initials: C
authors.lastname: Hansell
authors.forename: Robert
authors.initials: R
authors.lastname: Nibbs
mesh_terms: D000818:Animals; D018925:Chemokines / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D019707:Receptors, Chemokine / Q000502:physiology; D015398:Signal Transduction
chemical_list: D018925:Chemokines; D019707:Receptors, Chemokine