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.
Keywords: Blood-brain barrier, BBB; Hypoxia-ischaemia encephalopathy, HIE; Hypoxia-ischaemia, HI; Hypoxic-ischaemia; Immune response; Lymphocytes; Neonatal encephalopathy; Neonatal encephalopathy, NE; Regulatory T cells, Tregs; T cell receptors, TCRs; T helper, Th; Therapeutic hypothermia, TH; White Matter Injury, WMI; activating transcription factor-6, ATF6; central nervous system, CNS; granulocyte-macrophage colony-stimulating factor, GM-CSF; interleukin, IL; major histocompatibility complex, MHC; natural killer, NK cells; tumour necrosis factor-alpha, TNF-α.
© 2021 The Author(s).