Domino Effect of Interleukin-15 and CD8 T-Cell–Mediated Neuronal Apoptosis in Experimental Traumatic Brain Injury

Wu, Liang; Ji, Ningfei; Wang, Hang; Hua, Jingyu; Sun, Guolin; Chen, Pan‐Pan; Hua, Rong; Zhang, Yongmei

doi:10.1089/neu.2017.5607

Cited by 19 publications

(24 citation statements)

References 45 publications

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“…CD8 + T cells likely mediate their harmful effects and promote neuronal/myelin degeneration via GrB/perforin pathways. A recent TBI study found that CD8 + T cells infiltrated early at 24 h (promoted by astrocyte-derived IL-15) and secreted GrB, causing the activation of caspase-3/poly ADP ribose polymerase (PARP) pathways, which led to neuronal apoptosis (Wu et al, 2018). Increased GrB expression (which correlated with infiltrated CD8 + T cells) has also been observed in a rat model of SCI (Chaitanya et al, 2009) and ischemic stroke (Chaitanya et al, 2010).…”

Section: Discussionmentioning

confidence: 98%

Activated CD8+ T Cells Cause Long-Term Neurological Impairment after Traumatic Brain Injury in Mice

et al. 2019

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Section: Discussionmentioning

confidence: 98%

Activated CD8+ T Cells Cause Long-Term Neurological Impairment after Traumatic Brain Injury in Mice

et al. 2019

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“…The contribution of CD8 + T cells in the CNS post‐traumatic injury has been reported in several studies. After TBI, infiltrating CD8 + T cells in lesions were in close proximity to IL‐15‐expressing astrocytes, which subsequently release granzyme B; thus, activating caspase‐3 and cleaving poly‐ADP‐ribose polymerase and, ultimately, inducing neuronal apoptosis 55 . CD8 + T cells also produce TNF‐α and IFN‐γ to stimulate astrocytes to secrete inflammatory cytokines 56 .…”

Section: Cd8+ T Cells In the Cns Post‐traumatic Injurymentioning

confidence: 99%

“…How are the CD8 + T cells regulated at the wound site? On the one hand, the local cells, such as astrocytes, express IL‐15 and promote CD8 + T cells to release granzyme B 55 . On the other hand, possibly because of their negative effects, the body has some way of inhibiting them to reduce their adverse effects on damaged tissue.…”

Section: Cd8+ T Cells In the Cns Post‐traumatic Injurymentioning

confidence: 99%

T‐cell infiltration, contribution and regulation in the central nervous system post‐traumatic injury

Wang

et al. 2021

Cell Proliferation

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T cells participate in the repair process and immune response in the CNS post‐traumatic injury and play both a beneficial and harmful role. Together with nerve cells and other immune cells, they form a microenvironment in the CNS post‐traumatic injury. The repair of traumatic CNS injury is a long‐term process. T cells contribute to the repair of the injury site to influence the recovery. Recently, with the advance of new techniques, such as mass spectrometry‐based flow cytometry, modern live‐cell imaging, etc, research focusing on T cells is becoming one of the valuable directions for the future therapy of traumatic CNS injury. In this review, we summarized the infiltration, contribution and regulation of T cells in post‐traumatic injury, discussed the clinical significance and predicted the future research direction.

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“…8 Another important pathological response after TBI is neuronal 'programmed cell death', which leads to lifelong disability. [10][11][12] Thus, the drugs that reduce BBB disorders and alleviate apoptosis may decrease clinical complications and improve the prognosis of TBI. [10][11][12] Thus, the drugs that reduce BBB disorders and alleviate apoptosis may decrease clinical complications and improve the prognosis of TBI.…”

Section: Introductionmentioning

confidence: 99%

Dl‐3n‐butylphthalide improves traumatic brain injury recovery via inhibiting autophagy‐induced blood‐brain barrier disruption and cell apoptosis

et al. 2019

J Cellular Molecular Medi

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Blood-brain barrier (BBB) disruption and neuronal apoptosis are important pathophysiological processes after traumatic brain injury (TBI). In clinical stroke, Dl-3nbutylphthalide (Dl-NBP) has a neuroprotective effect with anti-inflammatory, anti-oxidative, anti-apoptotic and mitochondrion-protective functions. However, the effect and molecular mechanism of Dl-NBP for TBI need to be further investigated.Here, we had used an animal model of TBI and SH-SY5Y/human brain microvascular endothelial cells to explore it. We found that Dl-NBP administration exerts a neuroprotective effect in TBI/OGD and BBB disorder, which up-regulates the expression of tight junction proteins and promotes neuronal survival via inhibiting mitochondrial apoptosis. The expressions of autophagy-related proteins, including ATG7, Beclin1 and LC3II, were significantly increased after TBI/OGD, and which were reversed by Dl-NBP treatment both in vivo and in vitro. Moreover, rapamycin treatment had abolished the effect of Dl-NBP for TBI recovery. Collectively, our current studies indicate that Dl-NBP treatment improved locomotor functional recovery after TBI by inhibiting the activation of autophagy and consequently blocking the junction protein loss and neuronal apoptosis. Dl-NBP, as an anti-inflammatory and anti-oxidative drug, may act as an effective strategy for TBI recovery.Fangfang Wu and Ke Xu contributed equally to this work. | 1221WU et al.

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Domino Effect of Interleukin-15 and CD8 T-Cell–Mediated Neuronal Apoptosis in Experimental Traumatic Brain Injury

Cited by 19 publications

References 45 publications

Activated CD8+ T Cells Cause Long-Term Neurological Impairment after Traumatic Brain Injury in Mice

Activated CD8+ T Cells Cause Long-Term Neurological Impairment after Traumatic Brain Injury in Mice

T‐cell infiltration, contribution and regulation in the central nervous system post‐traumatic injury

Dl‐3n‐butylphthalide improves traumatic brain injury recovery via inhibiting autophagy‐induced blood‐brain barrier disruption and cell apoptosis

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