Antibody targeting of the CC chemokine ligand 5 results in diminished leukocyte infiltration into the central nervous system and reduced neurologic disease in a viral model of multiple sclerosis.

摘要: Intracerebral infection of mice with mouse hepatitis virus, a member the Coronaviridae family, reproducibly results in an acute encephalomyelitis that progresses to chronic demyelinating disease. The ensuing neuropathology during stage disease is primarily immune mediated and similar human multiple sclerosis. Secretion chemokines within CNS signals infiltration leukocytes, which destruction white matter neurological impairment. CC chemokine ligand (CCL)5 localized tracts undergoing demyelination, suggesting this participates pathogenesis by attracting inflammatory cells into CNS. In study, we administer mAb directed against CCL5 established virus-induced demyelination impaired motor skills. Anti-CCL5 treatment decreased T cell accumulation based, part, on viral Ag specificity, indicating ability differentially target select populations cells. addition, administration anti-CCL5 improved function significantly (p ≤ 0.005) reduced severity macrophage These demonstrate can be through use neutralizing model demyelination.