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NEUROLOGY 1996;47:1542-1545
© 1996 American Academy of Neurology

T-cell subpopulations in the cerebrospinal fluid and peripheral blood of patients with multiple sclerosis

A follow-up study

O. Oksaranta, MD, S. Tarvonen, MD, J. Ilonen, MD, K. Poikonen, MSc, M. Reunanen, MD, M. Panelius and R. Salonen, MD

From Turku Immunology Centre and Departments of Neurology (Drs. Oksaranta, Tarvonen, and Salonen, and M. Panelius) and Virology (Drs. Ilonen and Salonen), University of Turku, Turku, and the Departments of Medical Microbiology (K. Poikonen) and Neurology (Dr. Reunanen), University of Oulu, Oulu, Finland.
Supported by Sigrid Juselius Foundation and the University of Turku Foundation.
Received March 7, 1996. Accepted in final form May 6, 1996.
Address correspondence and reprint requests to O. Oksaranta, University of Turku, Department of Neurology, Kiinanmyllynkatu 13, FIN-20520 Turku, Finland.

We analyzed the relative and absolute numbers of CD4+ cells positive and negative for CD45RA marker as well as the numbers of CD8+ cells positive and negative for CD11b in the cerebrospinal fluid (CSF) and peripheral blood (PB) of 17 patients with multiple sclerosis (MS) during and 60 days after an exacerbation.We also studied samples from 27 control patients, 17 of whom had a noninflammatory neurologic disease and 10 of whom had an inflammatory neurologic disease other than MS. The results confirmed the small number of CD45RA-positive (naive or suppressor inducer) CD4+ cells as well as CD11b-positive (suppressor) CD8+ cells in the CSF compared with the PB for all paired CSF-blood comparisons. The relative numbers of these cells did not significantly differ between samples taken during an exacerbation and those taken 2 months later. In PB, the percentage of CD8+ CD11b-positive lymphocytes was lower in patients with MS or in patients with an inflammatory neurologic disease than in patients with a noninflammatory neurologic disease. The results indicate that there are fewer cells responsible for suppression-related phenomena in CSF than in PB but that this phenomenon is not specific to MS.

NEUROLOGY 1996;47: 1542-1545






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