CCR5 deficiency does not prevent P0 peptide 180–199 immunized mice from experimental autoimmune neuritis

Neurobiology of Disease

Zhiguo Chen¹  Bengt Winblad¹  Hernan Concha Quezada²  Lei Bao³  Jie Zhu³  Inger Nennesmo⁴  Rui-Sheng Duan⁴ 

[1] Center for Infectious Medicine, Department of Medicine, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden;Department of Neurology, the First Hospital, Jilin University, Changchun, China;Division of Pathology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden;Division of Experimental Geriatrics, Department of Neurotec, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden;

关键词: CCR5;    Experimental autoimmune neuritis;    Guillain–Barré syndrome;    IP-10;    MIP-1β;   

DOI  :  

来源: DOAJ

【 摘 要 】

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-1β 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-1β and IP-10 in sciatic nerves may compensate the CCR5 deficiency and contribute to inflammatory cells infiltrating to the PNS.

【 授权许可】

Unknown