title: CCR5 deficiency does not prevent P0 peptide 180-199 immunized mice from experimental autoimmune neuritis.
abstract: Experimental autoimmune neuritis (EAN) is an inflammatory autoimmune demyelinating disease of peripheral nervous system (PNS) and represents an animal model of Guillain-Barré syndrome (GBS) in man. The inflammatory cell infiltrating into the PNS is a prerequisite for developing EAN. To explore the role of CC chemokine receptor 5 (CCR5) in the inflammatory process of EAN, we induced EAN in CCR5-deficient (CCR5(-/-)) mice with P0 protein peptide 180-199. We found that CCR5(-/-) mice showed a similar EAN clinical course and severity as well as profile of infiltrating macrophages and T cells in cauda equina (CE) of EAN and the same levels of spleen mononuclear cell (MNC) response to antigen and mitogen when compared with CCR5(+/+) control mice. However, increased IP-10 and MIP-1beta production in sciatic nerves were seen in CCR5(-/-) mice. These results suggest that CCR5 deficiency does not prevent P0 peptide 180-199-immunized mice from EAN. Increased MIP-1beta and IP-10 in sciatic nerves may compensate the CCR5 deficiency and contribute to inflammatory cells infiltrating to the PNS.
authors.affiliation: Division of Experimental Geriatrics, Department of Neurotec, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
authors.forename: Rui-Sheng
authors.initials: RS
authors.lastname: Duan
authors.forename: Zhiguo
authors.initials: Z
authors.lastname: Chen
authors.forename: Lei
authors.initials: L
authors.lastname: Bao
authors.forename: Hernan Concha
authors.initials: HC
authors.lastname: Quezada
authors.forename: Inger
authors.initials: I
authors.lastname: Nennesmo
authors.forename: Bengt
authors.initials: B
authors.lastname: Winblad
authors.forename: Jie
authors.initials: J
authors.lastname: Zhu
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D054407:Chemokine CCL4; D018925:Chemokines / Q000235:genetics; D015870:Gene Expression / Q000276:immunology; D020275:Guillain-Barre Syndrome / Q000276:immunology / Q000503:physiopathology; D007114:Immunization; D016753:Interleukin-10 / Q000378:metabolism; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D018993:Myelin P0 Protein / Q000276:immunology*; D009444:Neuritis, Autoimmune, Experimental / Q000276:immunology* / Q000503:physiopathology*; D012333:RNA, Messenger / Q000032:analysis; D019713:Receptors, CCR5 / Q000172:deficiency / Q000235:genetics*; D019707:Receptors, Chemokine / Q000235:genetics; D012584:Sciatic Nerve / Q000276:immunology / Q000503:physiopathology; D013154:Spleen / Q000502:physiology
chemical_list: D054407:Chemokine CCL4; D018925:Chemokines; D019402:Macrophage Inflammatory Proteins; D018993:Myelin P0 Protein; D012333:RNA, Messenger; D019713:Receptors, CCR5; D019707:Receptors, Chemokine; D016753:Interleukin-10