Severity of traumatic brain injury governs alterations in type 17 T helper cell subset composition

Immune cell hyperactivation along with cytokines they overproduce plays an important role in traumatic brain injury (TBI). A central place in the immunopathogenesis of TBI is held by diverse cell-mediated reactions governed by T helper (Th) cell populations including Th17 subset. We studied peripheral blood plasma samples of the patients with sarcoidosis (n = 123): group 1 – patients with concussion; group 2 – mild TBI; group 3 – moderate TBI; and group 4 – severe TBI. The control group was samples from healthy volunteers (n = 48). T cell subset composition was assessed by flow cytometry. Within Th central memory cells (Th CM): the level of “double-negative” Th17 (DN Th17) was significantly increased in patients with mild TBI (p = 0.014) and moderate TBI (p = 0.003); the level of “classical” Th17 (p = 0.010) also was significantly increased, but only with severe TBI; the level of “non-classical” Th 17 (Th17.1) were shown to have significantly reduced level only patients with severe TBI (p = 0.008); the level of “double-positive” Th17 (DP Th17) was significantly increased in patients with mild TBI (p = 0.006) and moderate TBI (p = 0.012). Within Th effector memory cells, an increased level of DN Th17 turned out to be significantly increased in all groups (p 0.05) and “classical” Th17 in patients with mild TBI and moderate TBI (р 0,05); the level of Th17.1 was significantly reduced in patients with severe TBI (p = 0.015). The results indicate the active generation of a subpopulation of Th17 cells of both central (Th CM) and effector memory (ThEM), which indicates directed migration of cells in response to TBI. This probably occurs due to the high plasticity of Th17 (changes in phenotype) and functional properties that change depending on the microenvironment into which a particular cell finds itself, which causes the occurrence of reciprocal changes as a response to damage in nervous tissue of different severity.