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

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.