Features of humoral immunity in patients with mild traumatic brain injury

Traumatic brain injury (TBI) is an important problem of the healthcare system. A lPeading role in pathogenesis belongs to action shock wave upon skull and integuments, extending from impacted site, as well displacement rotation cerebral hemispheres relative fixed stem. As a result, cascade metabolic, biochemical inflammatory changes initiated, leading secondary damage. TBI, depending on its mechanism, severity type, causes various primary structural functional lesions at molecular, cellular, tissue organ levels with dysregulation all systems body, dependent degree extent. In most cases, increases risk developing epilepsy neurodegenerative diseases such Alzheimers disease, arkinsons disease chronic traumatic encephalopathy (CTE), mental health disorders. TBI long-term symptomatic process patients response event, damage-associated molecular patterns (DAMPs) encountered damage are expressed, which cause activation resident cells, secretion multiple chemokine cytokine by distinct cell populations. Neutrophils migrate focal lesions, remove damaged cells debris. Migration T B observed 3-7 days after trauma. Hence, following injury, due immune reactions, more extensive lesion, so-called trauma, developed. The aim our study was evaluate mild injury.
 An increased number Bm2 IgDdimCD27low naive IgDlowCD27hi (plasmablasts) phenotype found contusion, compared comparison group. Moreover, mature CD27lowCD38dim significantly decreased controls.