Abstract

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

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