Abstract

Post-traumatic stress disorder in combat veterans has certain characteristics common to combatants. B lymphocytes may aggravate neurocognitive impairment by demonstrating a significant proinflammatory tendency through the production of immunoglobulins and a number of proinflammatory factors. Objective: to study the phenotypic heterogeneity of B lymphocyte subpopulations in veterans with post-traumatic stress disorder. Studies were conducted in a cohort of veterans of the special military operation in Ukraine (SVO), including 26 combatants with clinically verified PTSD who made up the main (1) group, and 30 veterans were included in the comparison group (2). The diagnosis was verified on the basis of neuropsychological and pathopsychological examination. Determination of IL-10 levels (pg/mL) using a multiplex analysis on a Luminex Magpix 100 immunoanalyzer (USA) using the Bio-Plex multiplex analysis test system (MERZ, Germany) was performed. Gating of the B lymphocyte population was performed on a Navios flow cytofluorimeter (Beckman Coulter, USA) using a standardized technology for assessing the lymphocyte component of immunity. In the group of SVO veterans with PTSD, we showed an increase in blood cells with the CD45+CD3-CD19+CD5+ phenotype in comparison with the indicators of groups 2 and 3. B lymphocytes expressing the CD5+ marker are found in various human tissues and can also produce autoantibodies. Analysis of subpopulations of B lymphocytes with markers of memory cells showed a significant decrease in the blood of SVO veterans in the total number of memory B lymphocytes (CD45+CD3-CD19+CD27+), against the background of an increase in the concentration of cells positive for CD5 and CD27 with the phenotype CD45+CD3-CD19 +CD5+CD27+CD27+. B cells play a critical role in the mechanisms of intercellular interaction. The phenotypic diversity of B lymphocyte subpopulations that we have established in veterans with post-traumatic stress disorder is characterized by an increase in the circulation of B lymphocytes with CD5 and CD27 molecules, against the background of a general decrease in memory B cells. This indicates a possible autoimmune orientation of neuroinflammatory processes in the brain, associated both with a stress-induced increase in the permeability of the blood-brain barrier, and with the need to control excessive activation of immunocompetent cells.

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