The paper presents data on the study of the content of cytokines (IL-1β, RAIL-1β, IL-2, IL-4, IL-10, IL-17A, TNF-, IFN-γ) in the morning urine using enzyme immunoassay in healthy individuals (n = 20) and in patients with acute glomerulonephritis (n = 93). The determination of cytokine levels in patients was carried out in the debut of the disease and 12 months after the onset of the disease. The obtained indicators of cytokine content in the urine are presented as absolute values in pg/ml and creatinine-normalized values calculated by the formula: cytokine level (pg/ml) / urine creatinine (µmol/ml). The study was made of changes in the content of cytokines in the urine of patients with glomerulonephritis with respect to a group of healthy individuals, as well as the dynamics of the content of cytokines in the urine during the 12-month observation period. The results of the study showed that the absolute values of cytokines in urine can distort the true picture of the cytokine profile of urine in renal pathology. Normalized values of the predominant number of pro- and anti-inflammatory cytokines (IL-1β, IL-2, IL-8, IL-10, IL-17A and TNF-α) in patients with glomerulonephritis were significantly higher than the corresponding indicators of healthy individuals. The normalized values of cytokines were shown to be as more sensitive indicators than absolute values in the course of analyzing differences in the cytokine profile in patients with glomerulonephritis, depending on chronic and acute course of the disease. These indicators influenced the outcome of glomerulonephritis, assessed, as a rule, 12 months after the onset of the disease. Thus, the low levels of IL-1β, IL-8 and IL-17А detected in the debut of the disease in combination with the high level of RAIL-1β determined the chronization of glomerulonephritis. So, the creatinine-normalized cytokine levels in the urine expand the possibilities of using the evaluation of the cytokine profile of urine to establish changes in the cytokine content in the urine in renal pathology and predict the chronization of glomerulonephritis.

Liver cirrhosis continues to be an acute problem of modern medicine due to the high rates of its prevalence and mortality. The high mortality rate is caused by the development of the number of life–threatening complications in decompensated forms of liver cirrhosis – hepatorenal syndrome, infections and varicose bleeding. Hepatorenal syndrome and infections are the result of immunological shifts occurring during decompensation of liver cirrhosis. Currently available literature data do not allow us to create a complete picture of the functional state of various links of adaptive immunity with decompensated liver cirrhosis. The aim of the research was to study the characteristic features of adaptive immunity in patients with decompensated liver cirrhosis. Material and methods. The prospective cohort study included 136 patients with decompensated liver cirrhosis, who received inpatient treatment in the hepatological department of the multidisciplinary hospital. The cohort of examined patients was divided into two groups, one of which included patients with liver cirrhosis of viral origin (n = 78), the other – patients with alcoholic liver cirrhosis (n = 58). In addition to the generally accepted standard methods, the patient examination program included immunological tests: identification of T- and B-lymphocytes, immunoregulatory and activated subpopulations of T-lymphocytes by the method of immunophenotyping peripheral blood mononuclear cells using monoclonal antibodies. The serum levels of immunoglobulins IgM, IgG, IgA, circulating immune complexes were determined by immunoturbidimetric method. Results. The study of indicators of the humoral link of adaptive immunity revealed an increase in the number of B cells, an increase in IgM, IgG, IgA and circulating immune complexes in patients with decompensated liver cirrhosis. The cellular link of adaptive immunity was characterized by an increase in the relative content of T helper cells, activated T cells against the background of a decrease in the number of immature T cells and T regulatory cells. Conclusions. The distinctive features of adaptive immunity in patients with decompensated liver cirrhosis are simultaneous activation of both humoral and cellular components, which, apparently, supports the systemic inflammatory process and the associated progressive liver fibrosis.

No abstract

In recent years, primary immunodeficiencies have turned from the class of rare diseases to the category of more common disorders which may be encountered by doctors of any clinical discipline. The first case of primary immunodeficiency disorder (PID) in Chuvashia was detected in 1993. Since that time, the Department of Internal Diseases with the Course of Clinical Immunology at the I. Ulyanov Chuvash State University registered all the cases of PID diagnosed in the region, introducing them into the Republican Registry of PID. The study was aimed for searching epidemiological indexes, clinical and laboratory manifestations of PID in Chuvash region. The study was based on the patient data obtained by retrospective analysis of 85 case histories of PID patients, treated at different departments of the Republican Clinical Hospital, and the City Chuvash Pediatric Clinical Hospital of Public Health Ministry in 2000-2019, as well as on 49 outpatient records of the patients included into the Regional PID Registry. Various forms of PIDs were diagnosed according to the criteria developed by the European Society for Immunodeficiency and the Pan-American Group on Immunodeficiency (1999). The results of this study showed that the incidence of PID in the Chuivash Region is 3.4:100,000. The incidence of common variable immune deficiency (CVID), the most common form of PID in the region, was 1.58 per 100,000 population. The average age at the time of CVID diagnosis in Chuvash patients was 30.4±16.1 years, and the age of CVID debut was 11.3±15.0 years. The delay in proper diagnosis from the moment of clinical manifestation of CVID was, on average, 17.9 years in the region. At the time of CVID diagnosis, the patients showed marked decrease in the levels of 3 or 2 immunoglobulin classes (IgG and IgA), and T-helper cell contents (CD3+CD4+) in peripheral blood. Prevalence of selective IgA deficiency with сlinical symptoms was 0.83 per 100,000 population of the region, and the incidence of the asymptomatic form of this PID was 1 : 167. In patients with selective IgA deficiency, there were also disorders in the T cell system manifesting as decreased relative number of cytotoxic T-cells as well as elevated IgG and IgM levels. The age of diagnosis of X-linked agammaglobulinemia in the region was 3.5±3.0 years. In addition to disturbances of humoral adaptive immunity in children with this disease, a decrease in absolute T cell numbers was detected. In conclusion, the article describes disturbances of postvaccinal immunity in a pregnant patient with CVID, with asymptomatic clinical course, thus leading to false interpretation of the serological markers of TORCH infections and wrong strategy of pregnancy management.

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-