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Implications of immune responses for stroke injury and recovery.

Brain Behav Immun. 2021 May 20:S0889-1591(21)00217-8. doi: 10.1016/j.bbi.2021.05.020. Epub ahead of print. PMID: 34023355.

Authors/Editors: Hermann DM, Liesz A, Dzyubenko E.
Publication Date: 2021


Via release of danger-associated molecular patterns (DAMPs), which are sensed by innate immune cells, stroke is a potent trigger of immune responses. Blood-derived leukocytes, namely polymorphonuclear neutrophils, monocytes/ macrophages, T and B cells, rapidly enter the brain post stroke in a coordinated manner. Persistent immune responses are noted over several weeks. Immune cells efficiently coordinate the removal of irreversibly injured cells from the brain parenchyma. At the same time, immune cells may induce bystander injuries, resulting in the exacerbation of brain infarcts in the acute stroke phase and disturbed brain remodeling associated with secondary neurodegeneration in the chronic phase. With the shift of focus from the acute to post-acute stroke phase, these detrimental effects of immune responses have turned out as major contributors to persistent behavioral deficits and long-term disability. This observation at the same time implies that manipulating immune responses might allow for efficiently enhancing stroke outcome even far in the post-acute stroke phase. In this special issue, we would like to elucidate the role of immune cells and immune signals in ischemic injury and brain remodeling, defining how immune responses might therapeutically be targeted for improving structural brain remodeling and functional neurological recovery.

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