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- W2562786224 abstract "OBJECTIVE: Testing Th17 cells for their eligibility as biomarker allowing identifying patients at risk to develop MS-reactivation after natalizumab (NAT)-cessation. BACKGROUND: MS patients switching immunotherapy from NAT are at risk to develop recurrence or rebound disease activity. Mechanisms that govern breakthrough disease are not well understood and, so far, suitable biomarkers are not available. Possible immunological scenarios that might contribute to MS reactivation after NAT-withdrawal include the facilitated entrance of potentially harmful immune cells such as proinflammatory effector T helper 17 (Th17) cells which have been acknowledged as crucial mediators of autoimmune tissue damage with a suggested pathogenic role in MS. DESIGN/METHODS: Study was enrolled with 57 patients exposed to NAT due to highly active MS. Blood samples were serially taken during NAT-therapy, during wash-out, and after resuming immunotherapy with fingolimod or dimethyl fumarate. Th17 cells and IL-17 were monitored by multi-colour flow cytometry and ELISA in blood and - when available - in cerebrospinal fluid (CSF). RESULTS: Relative numbers of Th17 cells and IL-17 levels were increased in blood of patients undergoing NAT-treatment. After NAT-cessation Th17- and IL-17 plasma levels dropped back to baseline. Of note, concentrations of Th17 cells and IL-17 were further decreased and almost undetectable in most blood sample obtained from individuals who experienced a relapse during washout, whereas high levels of IL-17 were detectable in parallel CSF samples available from those patients. CONCLUSIONS: Our finding might point to a facilitated re-entry of Th17 cells into the CNS prompted by the interrupted VLA4 blockade on trafficking lymphocytes, suggesting that assessment of the Th17/IL-17 axis might prove to be an applicable predictive marker of rebound MS activity in patients switching immunotherapies.Supported by grants of the German Ministry for Education and Research (“German Competence Network Multiple Sclerosis” (KKNMS), B1 Alliance. Disclosure: Dr. Wildemann has received personal compensation for activities with Biogen Idec, Merck Serono, Teva Neuroscience, and Genzyme Corporation. Dr. Schwarz has nothing to disclose. Dr. Korporal-Kuhnke has nothing to disclose. Dr. Haas has nothing to disclose." @default.
- W2562786224 created "2017-01-06" @default.
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- W2562786224 date "2016-04-05" @default.
- W2562786224 modified "2023-09-26" @default.
- W2562786224 title "Dynamics of Th17 Cells during and after Cessation of Natalizumab Therapy (P5.277)" @default.
- W2562786224 hasPublicationYear "2016" @default.
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