title: Central Nervous System and Peripheral Expression of CCL19, CCL21 and Their Receptor CCR7 in Experimental Model of Multiple Sclerosis.
abstract: It is well documented that inflammatory chemokines play a significant role in the development of multiple sclerosis (MS) and its model, experimental autoimmune encephalomyelitis (EAE). Recently, the involvement of homeostatic (or lymphoid) chemokines in the pathogenesis of autoimmune diseases has become an object of intensive study. In this work, quantitative analysis of CCL19, CCL21 and CCR7 expression in the central nervous system (CNS), as well as in inflammatory mononuclear cells isolated from several organs during the first attack, remission and the second attack of chronic-relapsing EAE (ChREAE), was performed. Using real-time PCR, RNAse Protection Assay and immunohistochemistry, the expression of both chemokines, as well as of their common receptor CCR7, was analyzed in the brain, spleen, lymph nodes and peripheral blood mononuclear cells. Increased expression of CCL19 and CCL21 was observed mostly in mononuclear inflammatory cells isolated from the CNS during active ChREAE. At the same time the expression of CCR7 in blood mononuclear leukocytes was reduced. This observation extends our current knowledge about the possible role of chemokines CCL19, CCL21 and their receptor CCR7 in the pathogenesis of ChREAE and, by extension, MS.
authors.affiliation: Department of Neurology and Stroke, Medical University of Lodz, Lodz, Poland. bartosz.bielecki@inserm.fr.|U1195 Inserm and University Paris-Sud, 80 General Leclerc st., 94276, Le Kremlin-Bicetre, France. bartosz.bielecki@inserm.fr.
authors.forename: Bartosz
authors.initials: B
authors.lastname: Bielecki
authors.affiliation: Department of Propedeutics of Neurology, Medical University of Lodz, Lodz, Poland.
authors.forename: Izabela
authors.initials: I
authors.lastname: Jatczak-Pawlik
authors.affiliation: Department of Propedeutics of Neurology, Medical University of Lodz, Lodz, Poland.
authors.forename: Pawel
authors.initials: P
authors.lastname: Wolinski
authors.affiliation: Department of Molecular Cancerogenesis, Medical University of Lodz, Lodz, Poland.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Bednarek
authors.affiliation: Department of Neurology and Stroke, Medical University of Lodz, Lodz, Poland.|Department of Propedeutics of Neurology, Medical University of Lodz, Lodz, Poland.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Glabinski
mesh_terms: D000818:Animals; D001921:Brain / Q000276:immunology*; D054415:Chemokine CCL19 / Q000235:genetics / Q000378:metabolism; D054421:Chemokine CCL21 / Q000235:genetics / Q000378:metabolism; D018450:Disease Progression; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008297:Male; D051379:Mice; D009103:Multiple Sclerosis / Q000276:immunology*; D054400:Receptors, CCR7 / Q000235:genetics / Q000378:metabolism
chemical_list: C515371:Ccr7 protein, mouse; D054415:Chemokine CCL19; D054421:Chemokine CCL21; D054400:Receptors, CCR7
keywords: Chemokine; Chemokine receptor; Experimental autoimmune encephalomyelitis; Neuroinflammation