2022
DOI: 10.1016/j.pneurobio.2022.102335
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Negative effects of brain regulatory T cells depletion on epilepsy

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Cited by 10 publications
(15 citation statements)
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“…These findings implied that Treg depletion promoted the development of a microglia‐mediated inflammatory environment after SCI. Similarly, recent studies have reported that Treg depletion almost completely abrogated the protective mechanisms against injury, through enabling TNFα, IL‐1β, IL‐6, and IL‐17 levels to increase rapidly 57 . Conversely, the expansion of brain‐resident Tregs protects against pathological neuroinflammation 58 .…”
Section: Discussionmentioning
confidence: 93%
“…These findings implied that Treg depletion promoted the development of a microglia‐mediated inflammatory environment after SCI. Similarly, recent studies have reported that Treg depletion almost completely abrogated the protective mechanisms against injury, through enabling TNFα, IL‐1β, IL‐6, and IL‐17 levels to increase rapidly 57 . Conversely, the expansion of brain‐resident Tregs protects against pathological neuroinflammation 58 .…”
Section: Discussionmentioning
confidence: 93%
“…The number of Tregs in the brain was negatively correlated with seizure frequency in patients with epilepsy ( 44 ). Depletion of intracerebral Tregs promoted astrocytosis, microglia, inflammatory cytokine production, oxidative stress and neuronal loss in the hippocampus after status epilepticus seizures ( 45 ). Modulation of Tregs in epileptic brain tissue has therapeutic potential.…”
Section: Discussionmentioning
confidence: 99%
“…In the development of TLE, the involvement of OS and neuroinflammation have been well established as important factors, in part because the large amount of energy required by the brain is considered to be a possible mechanism involved in epileptogenesis [ 12 , 21 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 ]. In recent studies, it was observed that the specific inhibition of NADPH oxidase (NOX), the main producer of OS through O 2 •− synthesis, modified chronic epilepsy in a TLE rat model, preventing ROS generation, mitochondrial depolarization, and neuronal death.…”
Section: Discussionmentioning
confidence: 99%