Expression of T subsets and mIL-2R in peripheral blood of newborns with hypoxic ischemic encephalopathy

Wang, Jian; Qin, Lu

doi:10.1007/s12519-008-0028-4

Cited by 15 publications

(12 citation statements)

References 19 publications

(19 reference statements)

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“…However, in neonatal HI models, the infiltration of CD4 + and CD8 + T cells to the immature brain occurs in the delayed and tertiary phases, usually starting after 24 hours and with a peak at 1 week and 2 weeks after HI insult, respectively (Benjelloun et al , 1999; Winerdal et al , 2012). A clinical study has shown that blood mononuclear cells in newborns are still in a relatively undifferentiated status, with low expression of surface markers (Wang and Lu, 2008). Thus, the delayed infiltration of T lymphocytes into the injured brain of neonates may be due to the immaturity of lymphoid cells during this developmental stage.…”

Section: The Role Of Adaptive Immune Cells In Neonatal Hi Brain Inmentioning

confidence: 99%

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Concepcion

Meng

et al. 2017

Progress in Neurobiology

179

189

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Perinatal hypoxia-ischemia remains the primary cause of acute neonatal brain injury, leading to a high mortality rate and long-term neurological deficits, such as behavioral, social, attentional, cognitive and functional motor deficits. An ever-increasing body of evidence shows that the immune response to acute cerebral hypoxia-ischemia is a major contributor to the pathophysiology of neonatal brain injury. Hypoxia-ischemia provokes an intravascular inflammatory cascade that is further augmented by the activation of resident immune cells and the cerebral infiltration of peripheral immune cells response to cellular damages in the brain parenchyma. This prolonged and/or inappropriate neuroinflammation leads to secondary brain tissue injury. Yet, the long-term effects of immune activation, especially the adaptive immune response, on the hypoxic-ischemic brain still remain unclear. The focus of this review is to summarize recent advances in the understanding of post-hypoxic-ischemic neuroinflammation triggered by the innate and adaptive immune responses and to discuss how these mechanisms modulate the brain vulnerability to injury. A greater understanding of the reciprocal interactions between the hypoxic-ischemic brain and the immune system will open new avenues for potential immunomodulatory therapy in the treatment of neonatal brain injury.

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Section: The Role Of Adaptive Immune Cells In Neonatal Hi Brain Inmentioning

confidence: 99%

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Concepcion

Meng

et al. 2017

Progress in Neurobiology

179

189

View full text Add to dashboard Cite

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“…During ischemia, neutrophils can amplify brain injury through inducing ROS production. Interestingly, however, studies have shown that lymphocytes play a negative role in the pathogenesis of the acute ischemic brain [31,32,33]. The main cytokines relating to the inflammatory responses seen in HIE are IL-1, IL-6, IL-10, TNF-α, and TGF-β, with high levels of these cytokines under oxidative stress correlating positively with HIE severity [34,35,36,37,38].…”

Section: Pathogenesis and Molecular Mechanismsmentioning

confidence: 99%

Oxidative Stress in Hypoxic-Ischemic Encephalopathy: Molecular Mechanisms and Therapeutic Strategies

Zhao

Zhu

Fujino

et al. 2016

IJMS

159

108

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Hypoxic-ischemic encephalopathy (HIE) is one of the leading causes of morbidity and mortality in neonates. Because of high concentrations of sensitive immature cells, metal-catalyzed free radicals, non-saturated fatty acids, and low concentrations of antioxidant enzymes, the brain requires high levels of oxygen supply and is, thus, extremely sensitive to hypoxia. Strong evidence indicates that oxidative stress plays an important role in pathogenesis and progression. Following hypoxia and ischemia, reactive oxygen species (ROS) production rapidly increases and overwhelms antioxidant defenses. A large excess of ROS will directly modify or degenerate cellular macromolecules, such as membranes, proteins, lipids, and DNA, and lead to a cascading inflammatory response, and protease secretion. These derivatives are involved in a complex interplay of multiple pathways (e.g., inflammation, apoptosis, autophagy, and necrosis) which finally lead to brain injury. In this review, we highlight the molecular mechanism for oxidative stress in HIE, summarize current research on therapeutic strategies utilized in combating oxidative stress, and try to explore novel potential clinical approaches.

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“…A small cohort study reported that human neonates who have suffered from asphyxia show an increase in T cells in the circulation up to day 3 after birth, with counts normalizing after 7 days (Wang & Lu 2008). This finding was supported by another study in which an increased αβ and γδ T cells was detected in neonates suffering from pre-term asphyxia (Krolak-Olejnik & Mazur 2004).…”

Section: Sex Differences In Ischemic Injury Before Pubertymentioning

confidence: 99%

Sex differences in stroke across the lifespan: The role of T lymphocytes

Bravo-Alegría

McCullough

2017

Neurochemistry International

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Stroke is a sexually dimorphic disease. Ischemic sensitivity changes throughout the lifespan and outcomes depend largely on variables like age, sex, hormonal status, inflammation, and other existing risk factors. Immune responses after stroke play a central role in how these factors interact. Although the post-stroke immune response has been extensively studied, the contribution of lymphocytes to stroke is still not well understood. T cells participate in both innate and adaptive immune responses at both acute and chronic stages of stroke. T cell responses also change at different ages and are modulated by hormones and sex chromosome compliment. T cells have also been implicated in the development of hypertension, one of the most important risk factors for vascular disease. In this review, we highlight recent literature on the lymphocytic responses to stroke in the context of age and sex, with a focus on T cell response and the interaction with important stroke risk factors.

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Expression of T subsets and mIL-2R in peripheral blood of newborns with hypoxic ischemic encephalopathy

Cited by 15 publications

References 19 publications

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Oxidative Stress in Hypoxic-Ischemic Encephalopathy: Molecular Mechanisms and Therapeutic Strategies

Sex differences in stroke across the lifespan: The role of T lymphocytes

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