Immunophenotyping of cerebrospinal fluid cells in virus-associated neurologic diseases

Abstract

OBJECTIVE: To characterize the cellular immunophenotype of cells in cerebrospinal fluid (CSF) of patients with virus-associated neurologic diseases. BACKGROUND: Various inflammatory neurologic diseases are associated with viral infections. These agents may cause direct damage of infected cells associated with immunological alterations such as chronic activation, immunodeficiency and infiltration of inflammatory cells into the CNS that underlie the pathogenesis of inflammatory neurologic diseases. Therefore, characterization of local immune responses that are associated with the inflammatory milieu may provide evidence or pathogenic “signature” of an immunopathogenic process in virus-associated neurologic diseases. DESIGN/METHODS: Multicolor flow cytometry is used to characterize CD4+ and CD8+ T cells, B cells, monocytes and NK cells in the CSF and blood of patients with virus-associated neurologic diseases including HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP; n=16), HIV adequately treated with antiretroviral drugs (n=16), multiple sclerosis (MS; n=4) and progressive multifocal leukoencephalopathy (PML; n=6) compared to healthy volunteers (n=6). RESULTS: In all patients, T cells were the predominant population in the CSF. CD4+ and CD8+ T cells were significantly altered among the groups, and the CD4/CD8 ratio reduced in HIV, HAM/TSP and a subset of PML, but elevated in MS. In patients with HAM/TSP, activated CD4+ T cells were significantly increased in the CSF as well as the blood and correlated with HTLV-1 proviral DNA loads. MS patients had a decreased frequency of effector/memory CD4+ and CD8+ T cells in the CSF. B cells and antibody producing plasma cells were elevated in patients with HAM/TSP, MS and PML whereas monocytes were reduced. CD56bright/CD56dim NK cell ratio was elevated in the CSF of patients with HAM/TSP. CONCLUSIONS: Immunophenotyping of CSF cells may reflect immune pathology in inflammatory neurologic diseases and can serve to highlight differential diagnoses that may lead to a better understanding of disease pathogenesis and clinical treatment. Disclosure: Dr. Akahata has nothing to disclose. Dr. Massoud has nothing to disclose. Dr. Caruso has nothing to disclose. Dr. Ohayon has nothing to disclose. Dr. Billioux has nothing to disclose. Dr. Von Geldern has nothing to disclose. Dr. Smith has nothing to disclose. Dr. Nath has nothing to disclose. Dr. Jacobson has nothing to disclose.