Mx proteins in blood leukocytes for monitoring interferon beta-1b therapy in patients with MS
To correlate Mx protein (Mx) levels in lysed blood leukocytes with the clinical response to interferon (IFN) beta-1b (IFNbeta-1b) in relapsing-remitting MS (RR-MS) patients for monitoring treatment. Intracellular Mx expression is exclusively induced by the type I IFNs (IFN-alpha, -beta, and -omega)...
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Published in: | Neurology Vol. 54; no. 1; pp. 193 - 199 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Hagerstown, MD
Lippincott Williams & Wilkins
11-01-2000
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Subjects: | |
Online Access: | Get full text |
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Summary: | To correlate Mx protein (Mx) levels in lysed blood leukocytes with the clinical response to interferon (IFN) beta-1b (IFNbeta-1b) in relapsing-remitting MS (RR-MS) patients for monitoring treatment.
Intracellular Mx expression is exclusively induced by the type I IFNs (IFN-alpha, -beta, and -omega) or by viruses and is strongly increased under IFN treatment. Quantitative determination of Mx allows objective assessment of biological effects of IFN.
Mx protein levels were measured in blood leukocyte lysates from IFNbeta-1b-treated RR-MS patients by ELISA and correlated to clinical parameters, including relapse rate and clinical deterioration.
In stable IFNbeta-1b-treated MS patients, Mx levels were significantly increased compared to patients with or without immunosuppressive treatment. In IFN-1b-treated MS patients during relapse, Mx levels were significantly lower than during stable phases of the disease. Mean values of Mx (MVMx) over time of treatment in patients with a reduction of relapse rate were significantly higher than in patients without response.
Mx levels in lysed blood cells may represent a useful surrogate marker for IFNbeta-1b activity corresponding to the clinical response during treatment of MS. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0028-3878 1526-632X |
DOI: | 10.1212/wnl.54.1.193 |