Cytokine levels in the cerebrospinal fluid and serum of patients with multiple sclerosis
Interleukin (IL) 1β, tumor necrosis factor alpha (TNFα, and IL-6 are cytokines which mediate cellular responses during immune activation and inflammation. In multiple sclerosis (MS) they might be responsible for T-cell activation (IL-1β), for demyelination (TNFα), and for immunoglobulin (Ig) synthes...
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Veröffentlicht in: | Journal of neuroimmunology 1991-04, Vol.32 (1), p.67-74 |
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Zusammenfassung: | Interleukin (IL) 1β, tumor necrosis factor alpha (TNFα, and IL-6 are cytokines which mediate cellular responses during immune activation and inflammation. In multiple sclerosis (MS) they might be responsible for T-cell activation (IL-1β), for demyelination (TNFα), and for immunoglobulin (Ig) synthesis (IL-6) within the central nervous system. We studied IL-1β, TNFα, and IL-6 levels in the cerebrospinal fluid (CSF) of 34 patients with MS, 43 patients with non-inflammatory neurological diseases (NIND), and 19 patients with inflammatory neurological diseases (IND).
IL-6 was found in the CSF of 29% of MS, 7% of NIND, and 47% of IND patients. TNFα was detected in the CSF of 23% of MS, 7% of NIND, and 29% of IND. CSF IL-6 and TNFα levels were significantly higher in MS and IND than in NIND. IL-1β was rarely detected in the CSF of any group. At least one cytokine was detected in 52% of MS CSF, 11% of NIND CSF, and 64% of IND CSF. In MS patients, no relationship was observed between the incidence or the amount of intrathecal IgG synthesis or oligoclonal bands and the presence of any cytokine.
We also evaluated cytokine levels in paired sera from 11 MS and 13 NIND patients. Low levels of IL-6 were detected in most sera from MS and NIND patients. TNFα was detected in only two MS sera, and IL-1β was undetectable in any sample. Our results indicate that increased CSF levels of the cytokines IL-6 and TNFα occur frequently in MS and IND, but there is no obvious relationship to intrathecal Ig synthesis. |
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ISSN: | 0165-5728 1872-8421 |
DOI: | 10.1016/0165-5728(91)90073-G |