Immunopathogenic mechanisms of primary glomerulonephritis

karzakova, L. M; Zhuravleva, N. V; Abdelgafur, A. Y; Kudryashov, S I; Nawar, A. M

doi:10.21608/jbaar.2021.175196

	Immunopathogenic mechanisms of primary glomerulonephritis
Journal of Bioscience and Applied Research
Article 2, Volume 7, Issue 2, June 2021, Page 45-58 PDF (386.14 K)
Document Type: Original Article
DOI: 10.21608/jbaar.2021.175196
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Authors
L. M karzakova ¹; N. V Zhuravleva²; A. Y Abdelgafur²; S I Kudryashov²; A. M Nawar²
¹Doctor of Medical Sciences, Head of the department of internal diseases, Chuvash state university; 15, Moscow avenue, Cheboksary, 428015, Russian Federation
²Chuvash State University named after I. N. Ulyanov "Ministry of Education and Science of the Russian Federation, 428015, Cheboksary, Russia
Abstract
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-glycan antibodies. (ICs) isolated from patients with membranous nephropathy contain the podocyte receptor of phospholipase A2 (PLA 2 R) and anti- (PLA 2 R) autoantibodies belonging to (IgG 4). The central link in the immunopathogenesis of minimal changes in nephropathy is the development of an immediate hypersensitivity reaction. The prevalence of activation of the cellular mechanism of adaptive immunity acts as the main mechanism for the development of focal segmental nephrosclerosis.
Keywords
Glomerulonephritis; innate immunity; cytokines; (T reg); (T eff )


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