Journal
ANNALS OF NEUROLOGY
Volume 69, Issue 2, Pages 408-413Publisher
WILEY
DOI: 10.1002/ana.22352
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Funding
- Novartis AG, Basel, Switzerland
- Swiss National Science Foundation [PP00B-114850]
- Swiss MS Society
- Accorda
- Actelion
- Allergan
- Allozyne
- Bayer Schering
- Biogen Idec
- Biogen-Dompe
- Boehringer Ingelheim
- Genmab
- GlaxoSmithKline
- Medicinova
- Merck Serono
- Novartis
- Roche
- Sanofi Aventis
- Santhera
- Teva Pharmaceuticals
- UCB Pharma
- Wyeth
- Helvea
- Mediservice
- CSL Behring
- European Community
- Genzyme
- Novartis Foundation
- Rubato Foundation
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T cells exit secondary lymphoid organs along a sphingosine1-phosphate (S1P) gradient and, accordingly, are reduced in blood upon fingolimod-mediated S1P-receptor (S1PR)-blockade. Serving as a model of adaptive immunity, we characterized cellular and humoral immune responses to influenza vaccine in fingolimod-treated patients with multiple sclerosis (MS) and in untreated healthy controls. Although the mode of action of fingolimod might predict reduced immunity, vaccine-triggered T cells accumulated normally in blood despite efficient Si PR-blockade. Concentrations of anti-influenza A/B immunoglobulin (Ig)M and IgG also increased similarly in both groups. These results indicate that fingolimod-treated individuals can mount vaccine-specific adaptive immune responses comparable to healthy controls. ANN NEUROL 2011;69:408-413
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