CCRL2 regulates M1/M2 polarization during EAE recovery phase. Issue 6 (7th January 2016)

• Record Type: Journal Article
• Authors: Mazzon, Cristina; Zanotti, Lucia; Wang, Li; Del Prete, Annalisa; Fontana, Elena; Salvi, Valentina; Poliani, Pietro Luigi; Sozzani, Silvano
• Is Part Of: Journal of leukocyte biology. Volume 99:Issue 6(2016)
• Page Start: 1027
• Page End: 1033
• Publication Date: 2016-01-07
• Subjects: atypical chemokine receptors -- chemokines -- macrophages -- microglia -- inflammation -- multiple sclerosis; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.3MA0915-444RR
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : CCRL2 in the control of inflammation and demyelination in EAE. Abstract: Chemokine (CC motif) receptor-like 2 is a 7-transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental autoimmune encephalitis is an autoimmune disorder that replicates the inflammatory aspects of multiple sclerosis. Chemokine (CC motif) receptor-like 2–deficient mice developed exacerbated, nonresolving disease with protracted inflammatory response and increased demyelination. The increased severity of the disease was associated with higher levels of microglia/macrophage activation markers and imbalanced M1/M2 polarization. Thus, chemokine (CC motif) receptor-like 2 is involved in the downregulation of central nervous system–associated experimental autoimmune encephalitis inflammation in the recovery phase of the disease. Therefore chemokine (CC motif) receptor-like 2 should be considered to be a molecule involved in the regulation of the inflammatory response associated with multiple sclerosis.