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J Neurol Sci. 2016 Sep 15;368:77-83. doi: 10.1016/j.jns.2016.06.039. Epub 2016 Jun 17.

Stroke induces specific alteration of T memory compartment controlling auto-reactive CNS antigen-specific T cell responses.

Author information

1
Department of Neurology (JK, SH, and AM), Charité Universitaetsmedizin, Charitéplatz 1, Berlin, Germany. Electronic address: juliane.klehmet@charite.de.
2
Department of Neurology (JK, SH, and AM), Charité Universitaetsmedizin, Charitéplatz 1, Berlin, Germany. Electronic address: sarah.hoffmann@charite.de.
3
Department of Orthopedics, Helios Klinikum Buch, Schwanebecker Chaussee 50, Berlin, Germany. Electronic address: gerrit.walter@helioskliniken.de.
4
Department of Medical Immunology (CM), Charité Universitaetsmedizin, Berlin, Germany; Department of Immunology (CM), Labor Berlin Charité Vivantes, Sylter Strasse 2, Berlin, Germany. Electronic address: christian.meisel@laborberlin.com.
5
Department of Neurology (JK, SH, and AM), Charité Universitaetsmedizin, Charitéplatz 1, Berlin, Germany. Electronic address: andreas.meisel@charite.de.

Abstract

Whether and when auto-reactivity after stroke occurs is still a matter of debate. By using overlapping 15mer peptide pools consisting of myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) we show increased frequencies of immunodominant MOG- and MBP T cell responses in acute ischemic stroke which were associated with reduced frequencies of naïve T cells as well as CD8+ TEMRA cells. Auto-reactive CNS antigen-specific T cells responses as well as alterations of T cell subpopulations normalized in long-term follow up after stroke. Our findings suggest that stroke-induced immunodepression might function as an adaptive mechanism in order to inhibit harmful and long-lasting CNS antigen-specific immune responses.

KEYWORDS:

Auto-reactive T cell; MBP; MOG; Stroke; T memory cell

PMID:
27538605
DOI:
10.1016/j.jns.2016.06.039
[Indexed for MEDLINE]

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