title: CCRL2 regulates M1/M2 polarization during EAE recovery phase.
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.
authors.affiliation: Department of Molecular and Translational Medicine, University of Brescia, Italy; and Humanitas Clinical and Research Center, Rozzano, Italy.
authors.forename: Cristina
authors.initials: C
authors.lastname: Mazzon
authors.affiliation: Humanitas Clinical and Research Center, Rozzano, Italy.
authors.forename: Lucia
authors.initials: L
authors.lastname: Zanotti
authors.affiliation: Humanitas Clinical and Research Center, Rozzano, Italy.
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Molecular and Translational Medicine, University of Brescia, Italy; and Humanitas Clinical and Research Center, Rozzano, Italy.
authors.forename: Annalisa
authors.initials: A
authors.lastname: Del Prete
authors.affiliation: Department of Molecular and Translational Medicine, University of Brescia, Italy; and.
authors.forename: Elena
authors.initials: E
authors.lastname: Fontana
authors.affiliation: Department of Molecular and Translational Medicine, University of Brescia, Italy; and.
authors.forename: Valentina
authors.initials: V
authors.lastname: Salvi
authors.affiliation: Department of Molecular and Translational Medicine, University of Brescia, Italy; and.
authors.forename: Pietro Luigi
authors.initials: PL
authors.lastname: Poliani
authors.affiliation: Department of Molecular and Translational Medicine, University of Brescia, Italy; and Humanitas Clinical and Research Center, Rozzano, Italy silvano.sozzani@unibs.it.
authors.forename: Silvano
authors.initials: S
authors.lastname: Sozzani
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D016764:Cell Polarity / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002490:Central Nervous System / Q000187:drug effects / Q000473:pathology; D045142:Cross-Priming / Q000276:immunology; D018450:Disease Progression; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000473:pathology*; D005260:Female; D007114:Immunization; D007249:Inflammation / Q000473:pathology; D007371:Interferon-gamma / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017628:Microglia / Q000187:drug effects / Q000378:metabolism; D009186:Myelin Sheath / Q000378:metabolism; D063308:Myelin-Oligodendrocyte Glycoprotein / Q000276:immunology; D010446:Peptide Fragments / Q000276:immunology; D054388:Receptors, CCR; D019707:Receptors, Chemokine / Q000378:metabolism*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology
chemical_list: D000941:Antigens; C111851:Ccrl2 protein, mouse; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; D054388:Receptors, CCR; D019707:Receptors, Chemokine; C445081:myelin oligodendrocyte glycoprotein (35-55); D007371:Interferon-gamma
keywords: atypical chemokine receptors; chemokines; inflammation; macrophages; microglia; multiple sclerosis