Interferon gamma as a trigger of chronic viral infections and inflammatory dermatoses

Abstract

Interferon-gamma (IFN-γ) is the only representative of the type II interferon family regulating Th1 and Th2 immune responses. The discovery of IFN-γ is associated with the name of E. Frederick Wheelock. The expression of the IFNG gene provides a pleiotropic effect for IFN-γ, the main immune directions of this cytokine are antiviral, antibacterial and antiprotozoal. Unfortunately, in publications devoted to the relationship between the severity of inflammatory dermatoses (psoriasis, seborrheic dermatitis, atopic dermatitis) and levels of interferon gamma production, there is no consensus on the direct unity of these events. Although in most cases with acute viral diseases, an increase in interferon production is noted at the initial stages, but in some acute respiratory viral infections, its increase is not recorded (COVID-19, etc.), in cases of chronic viral diseases caused by retroviral infections – human immunodeficiency virus, human type 1 T-lymphotropic virus and endogenous human retroviruses as a result of prolonged exposure to IFN-γ on tissues, their damage may be noted, as well as a change in the functional state of CD4+ T cells. In cases of diseases caused by the herpes simplex virus 2, IFN-γ also has a complex effect on the intercellular relationships of infected and uninfected keratinocytes, as well as on the processes of apoptosis in Langerhans cells migrating to the dermis, which causes a violation of CD4+ and CD8+ involvement in the focus+ T-lymphocytes. In autoimmune diseases, IFN-γ can have a multidirectional effect. In particular, in patients with multiple sclerosis, IFN-γ regulates the processes of neuroinflammation and, depending on the concentration, can either reduce the number of CD11b+ myeloid cells of the central nervous system and reduce the infiltration of inflamed cells and normalize the processes of demyelination, or with an increase in IFN-γ production lead to reverse effects. At the same time, an enhancement of IFN-γ for transcription factors of differentially expressed genes in the case of systemic lupus erythematosus in patients has been proven.