Regulatory T cells are key cerebroprotective immunomodulators in acute experimental stroke

By Arthur Liesz, E. Suri‐Payer, C. Veltkamp, Henrike Doerr, C. Sommer, S. Rivest, T. Giese, R. Veltkamp. Nature Medicine, 2009

1,033 citations recorded by the source corpus.

Subfields: Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/b2a01b45f4ed4ec44209af1d22884489faedceb4

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Citations in the corpus

Regulation of innate immune responses in the brain (2009, background): “However, this influx of immune cells into the CNS can also be a protective mechanism, as depletion of regulatory T cells profoundly increased the extent of delayed brain damage and the deterioration of function, and IL-10 produced by regulatory T cells can suppress TNF and IFNγ production in the bra”
The immunology of stroke: from mechanisms to translation (2011, background): “In contrast, T regulatory (T reg ) cells are protective in the late stage of cerebral ischemia, an effect evident only if the injury is smal”
Immune responses to stroke: mechanisms, modulation, and therapeutic potential. (2020, background): “For example, prior tolerization of Tregs specific to the brain antigen myelin oligodendrocyte glycoprotein (MOG) leads to IL-10–dependent neuroprotection after stroke (146).”
The role of inflammation in epilepsy (2010, neutral): “132,133 Indeed, whether microglia, macrophages and/or T cells are destructive or neuroprotective seems to depend on their activation status, which is orchestrated by the specific inflammatory environment.”
Microbiota Dysbiosis Controls the Neuroinflammatory Response after Stroke (2016, background): “Specifically, it was shown previously that Thelper cell polarization occurs very early after brain injury and the Treg/Th17 balance contributes to outcome within the first 3 d after stroke (Liesz et al., 2009a; Shichita et al., 2009; Kleinschnitz et al., 2010).”
Ischemia and reperfusion—from mechanism to translation (2011, result): “For example, a recent study using an experimental stroke model showed that depletion of T reg cells substantially increased delayed brain damage and caused a deterioration in functional outcom”
Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδT cells (2016, positive): “T reg appear in the ischemic tissue after the acute phase and confer neuroprotection by secreting the anti-inflammatory cytokine IL-10, an effect thought to be antigen independent 9,10 .”
IL-4 induces cathepsin protease activity in tumor-associated macrophages to promote cancer growth and invasion. (2010, methodology): “provide phenotypic characterization of macrophages using CD68 and Iba1 as markers (Kozakowski et al. 2009; Liesz et al. 2009).”
Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke. (2019, background): “Studies have also shown that IFN- confers barrier characteristics in cultured brain endothelial cells, which may be useful in reducing damage from ischemic stroke (107, 108).”
Cell Biology of Ischemia/Reperfusion Injury (2012, background): “In general, the recruitment and reparative actions of Treg cells commence 3–7 days after the insult (Gandalfo et al., 2009; Kinsey et al., 2009, 2010; Liesz et al., 2009).”
Inflammatory mechanisms in ischemic stroke: role of inflammatory cells (2010, background): “Absence of Treg cells augmented postischemic activation of resident and infiltrating inflammatory cells 784 Journal of Leukocyte Biology Volume 87, May 2010 www.jleukbio.org including microglia and T cells, the main sources of cerebral TNF- and IFN- [97, 98], respectively.”