Abstract
Neurons and glia respond to acute injury by participating in the CNS innate immune response. This involves the recognition and clearance of “not self ” pathogens and “altered self ” apoptotic cells. Phagocytic receptors (CD14, CD36, TLR–4) clear “not self” pathogens; neurons and glia express “death signals” to initiate apoptosis in T cells.The complement opsonins C1q, C3, and iC3b facilitate the clearance of apoptotic cells by interacting with CR3 and CR4 receptors. Apoptotic cells are also cleared by the scavenger receptors CD14, Prs-R, TREM expressed by glia. Serpins also expressed by glia counter the neurotoxic effects of thrombin and other systemic proteins that gain entry to the CNS following injury. Complement pathway and T cell activation are both regulated by complement regulatory proteins expressed by glia and neurons. CD200 and CD47 are NIRegs expressed by neurons as “don't eat me” signals and they inhibit microglial activity preventing host cell attack. Neural stem cells regulate T cell activation, increase the Treg population, and suppress proinflammatory cytokine expression. Stem cells also interact with the chemoattractants C3a, C5a, SDF-1, and thrombin to promote stem cell migration into damaged tissue to support tissue homeostasis.
Highlights
Acute ischemic brain infarction and traumatic brain injury share several pathological features, including the disruption of the Blood Brain Barrier (BBB) with entry of systemic inflammatory cells and circulating blood proteins into the brain parenchyma
Stem cells are able to divide into glial-like cells with “regulatory” and “protective” activities that support dying neurons and oligodendroglia, a function mediated by the expression of growth factors and immunoregulatory molecules that control the local innate immune response, a characteristic described as “therapeutic plasticity” [15]
The balance between the protective and destructive effects of the innate immune response against pathogens and brain injury has been termed “a double-edged sword”. (Wryss coray 2002). This balance must be critically regulated in order to promote conditions supportive of brain repair and allow the damaged brain to return to normal function
Summary
Acute ischemic brain infarction and traumatic brain injury share several pathological features, including the disruption of the Blood Brain Barrier (BBB) with entry of systemic inflammatory cells and circulating blood proteins into the brain parenchyma. The surviving resident brain cells (neurons and glia) are not “professional” immune cells, but contribute to the defence of the brain through the expression of the innate immune response, promoting the clearance of neurotoxic proteins and apoptotic cells from the Central Nervous System (CNS). This stimulates both tissue repair (resolution) and the rapid restoration of tissue homeostasis [3,4,5,6]. There is increasing evidence that host stem cells contribute to the immune regulation of tissue inflammation through their interaction with the same brain cells responsible for the CNS innate immune system response [4, 15,16,17]
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