Cytokine Status of T-cellular Immune Response Direction in Oncological and Non-oncological Pathology of the Brain

ABSTRACT

The aim of the study was to investigate the cytokine status in patients with brain tumors, compared with traumatic brain injuries. The serum levels of the main mediators of type I and II, providing the development of an immune response by a cellular or humoral pathway, were studied in ٢٦ patients with brain tumors (BT) and in ٣٩ patients with traumatic brain injury (TBI). The initial levels of the studied cytokines exceeded the norm in most patients (٧٦٪), with a few exceptions. In patients of both groups after treatment, the levels of serum cytokines concentrations remained almost at the same level, with the exception of a significant decrease in interleukin-٦ (IL-٦) and interleukin-١ receptor antagonist (raIL-١), as well as a tendency to decrease in IL-٨ levels in the TBI group. In the BT group, the most significant indicator was interferon-gamma (IFN-γ): its level decreased after treatment by almost ٢ times (p<٠.٠٥), without, however, reaching the norm. In these patients, after treatment, an insignificant tendency to a decrease in the serum concentration of raIL-١ was also observed. Thus, the disturbances of the parameters of the main mediators of types I and II – tumor necrosis factor-alpha (TNF-α), IFN-α, IFN-γ, IL-٤, IL-٦, IL-٨ and raIL-١ – are manifested both in significant suppression and in hyperproduction of some of them. The increased initial level of proinflammatory cytokines and their pronounced decrease by the end of treatment in TBI patients indicate a switch in the direction of the immune response from the initially dominant cellular Th-١ type to the humoral one, which, given the no less importance of the humoral immunity in the developing systemic inflammatory reaction in them, should perhaps be regarded as a favorable prognostic indicator. The absence of significant changes in the concentrations of most of the studied cytokines in BT patients may be a sign of the developing depletion of antitumor immunity resources, and, as a consequence, the areactivity of the immune system.