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Quantification of γδ T cells and HLA-DR+ NK cells does not predict emergence of new contrast enhancing lesions in MS patients suspending natalizumab treatment
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Biology Education Centre.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurology.ORCID iD: 0000-0002-7045-1806
2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 6, article id e0179095Article in journal (Refereed) Published
Abstract [en]

Background

Natalizumab (NTZ) is a drug that has been widely used in the treatment of multiple sclerosis (MS). NTZ is very effective in suppressing inflammation, but if treatment is suspended many patients will experience relapses.

Objective

To investigate if quantification of γδ T cells and HLA-DR+ NK cells could predict early disease reactivation after NTZ suspension.

Methods

Absolute counts of γδ T cells and HLA-DR+ NK cells in whole blood were determined with flow cytometry in fifteen patients treated with NTZ. NTZ treatment was then withdrawn and patients were followed with clinical visits and MR investigations.

Results

Patients with recurrent disease had higher absolute counts of γδ T cells 129 (+/- 156) cells/μl in comparison to patients with stable disease 50.0 (+/- 51.0) cells/mu l but the difference was not statistically significant and largely driven by outliers. Patients with recurrent and stable disease had similar absolute counts of HLA-DR+ NK cells.

Conclusion

Quantification of γδ T cells and HLA-DR+ NK cells could not predict active disease after NTZ suspension.

Place, publisher, year, edition, pages
2017. Vol. 12, no 6, article id e0179095
National Category
Neurology
Identifiers
URN: urn:nbn:se:uu:diva-329692DOI: 10.1371/journal.pone.0179095ISI: 000402875700046PubMedID: 28586378OAI: oai:DiVA.org:uu-329692DiVA, id: diva2:1148328
Available from: 2017-10-10 Created: 2017-10-10 Last updated: 2017-11-29Bibliographically approved

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