The low effectiveness of the existing ways of treatment of glomerulonephritis (GN) requires the development of new treatment methods and profound studying of mechanisms of development of (GN). A review of modern literature data indicates a relationship between the development of (GN) with infection and activation of various components of the immune response. Pathogen-associated molecular patterns of infectious pathogens act as "danger signals" that activate Toll-like receptors of innate immune cells, as a result, a cascade of intracellular chain reactions is triggered, causing the production of growth factors and cytokines. The cytokine environment determines the pathway of differentiation of (CD 4 + ) helper cells into (Th1), (Th2), (Th17), and regulatory T cells (T reg). According to published data, a key link in the (GN) immunopathogenesis is an imbalance in the ratio of the activity of subpopulations of T helper cells, manifesting inhibition activity of (T reg) on a background of activation of effector cells ( T eff ) -( Th1), (Th2), (Th17). The activity of (Th1), (Th17)-cells are realized in the cellular mechanisms of the immunopathogenesis of (GN), while (Th2)-cells provide activation of the humoral component of adaptive immunity and the production of antibodies involved in the formation of immune complexes (ICs). This is a general scheme of the immunopathogenesis of (GN), which has specific variations depending on the clinical and morphological form of (GN). In post-infectious (GN), the activation of the humoral link of adaptive immunity with the formation of (ICs) and their subsequent deposition in the capillaries of the glomeruli comes to the fore. A feature of the immune complex process in patients with (IgA) nephropathy is the formation of "nephritogenic" ICs containing abnormal (IgA) (with impaired glycosylation of the IgA molecule) and anti-
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