1. Stroke induces specific alteration of T memory compartment controlling auto-reactive CNS antigen-specific T cell responses
- Author
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Sarah Hoffmann, Gerrit Walter, Christian Meisel, Andreas Meisel, and Juliane Klehmet
- Subjects
Adult ,Male ,0301 basic medicine ,Enzyme-Linked Immunospot Assay ,Neuroimmunomodulation ,T cell ,Autoimmunity ,Peptide ,Brain Ischemia ,Myelin oligodendrocyte glycoprotein ,Interferon-gamma ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,T-Lymphocyte Subsets ,medicine ,Humans ,Stroke ,Aged ,Aged, 80 and over ,chemistry.chemical_classification ,biology ,Compartment (ship) ,Myelin Basic Protein ,Middle Aged ,Flow Cytometry ,medicine.disease ,Myelin basic protein ,030104 developmental biology ,medicine.anatomical_structure ,Neurology ,chemistry ,Immunology ,biology.protein ,Female ,Myelin-Oligodendrocyte Glycoprotein ,Neurology (clinical) ,Immunologic Memory ,030217 neurology & neurosurgery ,CD8 ,Follow-Up Studies - 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.
- Published
- 2016