![]() ![]() Their exact contribution to the pathogenesis of brain injuries is not entirely understood, but studies have shown that microglial activation can persist for years following TBI in humans ( 2). Microglia are resident immune sentinels that respond to nearly all inflammatory events within the CNS. Immune reactions do indeed have the means to cause damage, but they also play a critical role in promoting tissue repair and recovery following brain injury. Although a number of studies suggest that neuroinflammation is detrimental and inhibitory to neural regeneration following TBI, the failure of anti-inflammatory drugs to achieve a therapeutic benefit in human clinical trials supports a growing need to more carefully interrogate the duality of TBI-induced immunity. A major question in the field of TBI research is how the immune response influences the pathogenesis of brain injury and recovery. Signaling from DAMP receptors initiates local cytokine and chemokine production, which affects the immediate environment and provides a cue for peripheral immune infiltration ( 1). Microglia and resident macrophages immediately respond to injury after sensing damage-associated molecular patterns (DAMPs), such as the presence of adenosine triphosphate (ATP) or intracellular proteins that are released from damaged or dying cells. Damage to the CNS elicits inflammatory responses from resident microglia and macrophages, as well as peripheral immune cells, such as neutrophils, monocytes, and T cells. ![]() Traumatic brain injuries (TBIs) cause many reactions one of the most prominent is neuroinflammation. ![]()
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