The role of lymphocytes in neonatal encephalopathy
| Autor: | Derek G. Doherty, Nawal A.B. Taher, Ashanty M. Melo, Eleanor J. Molloy |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Chemokine
Therapeutic hypothermia TH interleukin IL Neurosciences. Biological psychiatry. Neuropsychiatry Inflammation Review Brain damage granulocyte-macrophage colony-stimulating factor GM-CSF Neonatal encephalopathy Regulatory T cells Tregs Proinflammatory cytokine tumour necrosis factor-alpha TNF-α T cell receptors TCRs Immune system natural killer NK cells medicine White Matter Injury WMI Lymphocytes Immune response General Environmental Science major histocompatibility complex MHC biology business.industry Neurodegeneration activating transcription factor-6 ATF6 Hypoxia-ischaemia encephalopathy HIE Hypoxic-ischaemia medicine.disease Neonatal encephalopathy NE Hypoxia-ischaemia HI central nervous system CNS Blood-brain barrier BBB Immunology biology.protein General Earth and Planetary Sciences medicine.symptom business T helper Th Infiltration (medical) RC321-571 |
| Zdroj: | Brain, Behavior, & Immunity-Health, Vol 18, Iss, Pp 100380-(2021) Brain, Behavior, & Immunity-Health |
| ISSN: | 2666-3546 |
| DOI: | 10.1016/j.bbih.2021.100380 |
| Popis: | Neonatal encephalopathy is a syndrome characterised by abnormal neurological function often caused by a hypoxic insult during childbirth. Triggers such as hypoxia-ischaemia result in the release of cytokines and chemokines inducing the infiltration of neutrophils, natural killer cells, B cells, T cells and innate T cells into the brain. However, the role of these cells in the development of the brain injury is poorly understood. We review the mechanisms by which lymphocytes contribute to brain damage in NE. NK, T and innate T cells release proinflammatory cytokines contributing to the neurodegeneration in the secondary and tertiary phase of injury, whereas B cells and regulatory T cells produce IL-10 protecting the brain in NE. Targeting lymphocytes may have therapeutic potential in the treatment of NE in terms of management of inflammation and brain damage, particularly in the tertiary or persistent phases. |
| Databáze: | OpenAIRE |
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