Abstract

Neonatal encephalopathy is a disorder characterised by abnormal neurological work often caused by a hypoxic offended during childbirth. Triggers such as hypoxia-ischemia result in the discharge of cytokines and chemokines actuating the infiltration of neutrophils, natural killer cells, B cells, T cells and innate T cells into the brain. In any case, the part of these cells in the development of the brain injury is poorly caught on. We review the mechanisms by which lymphocytes contribute to brain damage in NE. NK, T and innate T cells discharge proinflammatory cytokines contributing to the neurodegeneration within the auxiliary and tertiary stage of damage, whereas B cells and administrative T cells deliver IL-10 protecting the brain in NE. Targeting lymphocytes may have therapeutic potential within the treatment of NE in terms of management of inflammation and brain damage, especially in the tertiary or diligent stages.