Russian Journal of Immunology

Peer-review quarterly medical journal.

 

Editor-in-chief

Publisher

About

Founded in 1996.

“Russian Journal of Immunology” is a scientific and educational journal in the field of fundamental and clinical immunology, the purpose of which is to promote the scientific achievements of fundamental and clinical immunology for various fields of medicine, publish reviews, lectures, articles by leading domestic and foreign experts in the field of fundamental and experimental immunology, clinical immunology, allergology, immunodiagnosis and immunotherapy of infectious, allergic, autoimmune and oncological diseases.

 

Indexation

  • Russian Science Citation Index (Web of Sciences)
  • Russian Science Electronic Library (eLibrary.ru)
  • Google Scholar
  • Ulrich's Periodicals directory
  • WorldCat
  • Crossref

 


Types of accepted articles

  • reviews
  • systematic reviews and metaanalyses
  • original research
  • clinical case reports and series
  • letters to the editor
  • short communications
  • clinial practice guidelines

Publications

  • in English and Russian
  • quarterly, 4 issues per year
  • continuously in Online First
  • with NO Article Processing Charges (APC)
  • distribution in Open Access with the Creative Commons Attribution 4.0 International License (CC BY 4.0))

Announcements

 

Russian Journal of Immunology has been transferen to the Eco-Vector online publishing platform

Posted: 19.02.2022

From February 2022, the Russian Journal of Immunology has been transferen to the Eco-Vector online publishing platform. We would like to thank the Eco-Vector employees for prompt and high-quality content transfer. The journal archive and all services of the electronic editorial system are active and functional. We look forward to a long and fruitful cooperation!

 
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Current Issue

Vol 25, No 1 (2022)

Cover Page

Full Issue

REVIEWS

Macrophages in gouty inflammation
Malyshev I.Y., Chernysheva O.O., Kuznetsova L.V., Pikhlak A.E.
Abstract

Gout disorder is likely to be the most common cause of inflammatory arthritis. Hyperuricemia leads to formation of poorly soluble crystalline urate salts in tissues and joints, thus being etiological factor of the gout. The review summarizes modern views on the mechanisms of autoinflammation in gout disorder and it provides an outlook for the new treatment approaches. Inflammation in gout is related to phagocytosis of the urate crystals and the macrophagic NLRP3 inflammosome activation. This process consists of preliminary stage and proinflammatory cytokine generation phases. During the preliminary phase, soluble and crystalline urate salts initiate mRNA transcription for IL-1β and other proinflammatory cytokines precursors in macrophages, synthesis of NLRP3 inflammosome components, and formation of immune memory. Enhanced transcription of IL-1β and other cytokine precursors is implemented via PRAS49-AKT-mTOR signaling, IL- 1ra anti-inflammantory factor and TLR-MyD88-IRAK-NF-κB pathway; the enhanced synthesis of NLRP3 inflammasome components provided via the TLR-NF-κB pathway. The immune memory develops due to the epigenetic modifications, associated with (de-) acetylation and (de-) methylation of histones and DNA. During the next phase, the effect of soluble and crystalline urate salts upon macrophages promotes NLRP3 inflammosome activation, due to the following events: 1. К+, Cl- and Са2+ ionic currents shift; 2. lysosomic and mitochondrial damage, leading to the cathepsin B release and enhancement of reactive oxygen production, respectively; 3. NLRP3 relocation between the endoplasmic reticulum, Golgi complex and cytosol; 4. alteration of the NLRP3 structure due to auxiliary proteins attachment, phosphorylation, ubiquitination and acetylation. The NLRP3 inflammosome activity results into increased caspase 1 production which, in turn, produces IL-1β and pyroptotic pores proteins. The pyroptotic pores allow IL-1β passage, which further amplifies inflammation. During the pyroptosis, soluble and crystalline urate salts release from the cells, further increasing inflammation and tissue damage. Understanding the mechanisms of gout-associated inflammation helps us to formulate promising approaches to development of novel treatments. Macrophages are the key cells to crystal-induced inflammation development. Thus, new biothechnologies based on macrophage engineering may appear to be prospective in gout treatment. In this review, we have analyzed the prospects of M3 phenotype macrophages (AB-M3) usage in therapy, unlike M1 and M2 phenotypes, is able to produce anti-inflammatory cytokines in response to the inflammatory factors and, therefore, to inhibit crystal-induced inflammation. Meanwhile, unlike the anti-IL-1β medications, e.g., canakinumab, targeting a single end product of the gout inflammation (IL-1β), AB-M3 macrophages inhibit not only IL-1β production, but also a group of other inflammatory cytokines.

Russian Journal of Immunology. 2022;25(1):7-22
pages 7-22 views
Immune-hormonal imbalance in chemical cancerogenesis
Glushkov A.N.
Abstract

The present article deals with experimental and clinical aspects of immuno-hormonal interactions in chemical carcinogenesis i.e., formation of DNA-adducts with chemical carcinogens as a trigger of tumor initiation; synthesis of specific antibodies as markers of human exposure to environmental carcinogens; immunomodulation of chemical carcinogenesis by the specific antibodies in experimental studies; interactions of antibodies against environmental carcinogens with endogenous steroid hormones in human carcinogenesis; immunological interference and inversion of immuno-hormonal interactions by the action of antibodies against environmental carcinogens; immune stimulation of tumor progression in cancer patients. It is shown that antibodies specific to estradiol and progesterone participate in regulation of serum estradiol and progesterone levels in healthy women. Excessive production of antibodies against benzo[a]pyrene is associated with impaired physiological balance between the levels of antibodies to estradiol and progesterone, thus causing disturbed physiological balance between serum estradiol and progesterone. Immuno-hormonal imbalance promotes tumor initiation, its growth and progression. The new approaches to the personalized cancer immunoprediction and immune prevention are discussed. Coordinated synthesis of antibodies against benzo[a]pyrene and estradiol seems to reflect production of DNA-adducts with genotoxic metabolic effects of these compounds manifesting as synergistic carcinogenic effects upon the target cells. Hence, simultaneously increased levels of serum antibodies against benzo[a]pyrene and estradiol in healthy people may be considered an immunological marker of high oncological risk and an reason to use of new immunoprotective tools against polycyclic aromatic hydrocarbons and phytoestrogens. However, ability of these antibodies to raise the blood serum levels of environmental carcinogens and endogenous estradiol, as shown in vitro and in vivo, excludes the opportunity for active cancer immune prevention. Usage of anticarcinogen vaccines aimed for induction of protective secretory antibodies is likely to further increase high levels of procarcinogenic serum antibodies against benzo[a]pyrene and estradiol, followed by additional enhancement of immuno-hormonal imbalance and promotion of carcinogenesis. Development of probiotics transduced with genes encoding human antibodies against environmental carcinogens may present an alternative approach to cancer immune prevention. The antibodies produced by such probiotics would bind appropriate carcinogens and prevent their invasion into the organism, thus inhibiting emergence of DNA-adducts and suppressing synthesis of specific autoantibodies that may promote carcinogenesis. The aim is to substantiate the concept of immuno-hormonal imbalance for the carcinogen-induced hormone-dependent tumors.

Russian Journal of Immunology. 2022;25(1):23-36
pages 23-36 views

ORIGINAL ARTICLES

Enhanced homeostatic proliferation of t lymphocytes after cyclophosphamide injection in c57bl/6 mice
Grinko .K., Marzanova S.N., Donetskova A.D.
Abstract

Chemotherapeutic agents are used in medicine to treat cancer. They can damage immune system and lead to the secondary immunodeficiency. T cells are most severely affected during chemotherapy. Restoration of the T lymphocytes is an important topic in research to understand pathogenesis of damaging effects caused by cytostatics and searching ways to correct the resulting disorders. The aim of our study was to follow the process of T cell recovery, and to understand the role of its homeostatic proliferation. 33 female C57BL/6 mice were included into the experiment. The experimental group (25 mice) received a single injection of cyclophosphamide (Cy) at a dose of 125 mg/kg; the control group did not receive the drug. Biomaterials for the study were splenocytes isolated on days 5, 10, 20, 30 and 60 after the drug administration. Flow cytometry was used to measure the recovery of T helpers (CD3+CD4+) and cytotoxic T lymphocytes (CTL, CD3+CD8+), as well as their “age-related” phenotype assayed for naive (Tnaive) and central memory (Tcm) T cells. The level of homeostatic proliferation was determined by the Tnaive/Tcm ratio. The total amount of splenocytes, T helpers, CTLs and the CD4+/CD8+ ratio showed a statistically significant increase at the early terms after Cy administration (day 5). Further, a decrease in splenocytes and their subpopulations was observed. We found that the CTL subpopulation didn’t recover even 2 months after the drug administration and was more sensitive to the action of cyclophosphamide than the T helper subpopulation. We have also revealed that naive T helpers and naive CTLs are most susceptible to the Cy action; these subpopulations also failed to recover 60 days after the drug administration. At the same time, the amount of central memory T cells predominated by the end of the experiment, showing conversion of the T cell phenotype. Thus, we have shown an increase in homeostatic proliferation, along with conversion of naive T cell phenotype to the central memory T cells after Cy administration accompanied by deficiency of naive T cells. Such changes cause skewing of TCR repertoire. This shift may cause premature aging of immune system and increases the risk of autoimmune diseases.

Russian Journal of Immunology. 2022;25(1):37-46
pages 37-46 views
Concentration of anti-inflammatory cytokines in supernatants of peripheral blood cell cultures in children with autoimmune and infectious diseases
Krivolapova I.M., Pashnina I.A.
Abstract

Cytokines belong to the class of signaling molecules, being involved into regulation of proliferation, differentiation and effector functions of immunocompetent cells. The ratio of pro- and anti-inflammatory cytokines is important for development of any inflammatory process. IL-1ra, IL-4, IL-10 are among the most important anti-inflammatory cytokines. Their function is to limit and suppress immune response in inflammatory processes of any etiology. In this respect, the aim of this study was to evaluate production of the anti-inflammatory cytokines IL-1ra, IL-4 and IL-10 by peripheral blood cells in children with autoimmune and infectious diseases. Patients and methods: Pediatric parients (2-17 years old) participated in the study including those with juvenile idiopathic arthritis (n = 101); unspecified reactive arthropathy (n = 24); systemic lupus erythematosus (SLE, n = 14); chronic viral hepatitis C (n = 24). 33 healthy children (n = 33) comprised the control group. Heparinized blood samples were diluted with glutamine-containing medium RPMI-1640. Control samples were not treated by any stimulants, and the stimulated samples were supplied with phytohemagglutinin (20 mkg/ml). The samples of diluted blood were incubated for 24 hours (37 °C, 5% CO2). The supernates were frozen once. The concentrations of IL-1ra, IL-4 and IL-10 in these cell supernatants were determined by ELISA technique (Vector-Best, Russia). Results: It was found that the spontaneous production of anti-inflammatory cytokines (IL-1ra, IL-4 and IL-10) didn’t differ, or was lower in the groups of patients with SLE, juvenile idiopathic arthritis and hepatitis C if compared with control group. SLE is an autoimmune disease, whereas juvenile arthritis is of mixed autoimmune-autoinflammatory etiology. Chronic hepatitis C is a viral disease, but autoimmune responses may manifest at the chronic stage of the disorder. Decreased production of anti-inflammatory cytokines could be an evidence for autoimmune mechanisms of these diseases, despite their different etiology. More intensive spontaneous production of IL-1ra and IL-10 in children with unspecified reactive arthropathy may suggest some compensatory reactions which inhibit development of inflammation in this disorder. IL-1ra, IL-4 and IL-10 production in stimulated cultures didn’t differ between all groups of the patients, or it was lower in comparison with healthy children. Decrease cytokine production in groups of children with different diseases suggests exhausted functional reserve of immunocompetent cells caused by their chronic activation.

Russian Journal of Immunology. 2022;25(1):47-54
pages 47-54 views
Features of cytokine status of the newborns with seizures
Gurbanova G.M., Ragimova N.J.
Abstract

The aim of the present study was to assess the level of cytokines in newborn children of various gestational terms with seizures. A prospective, comprehensive study of 307 newborns of various gestational ages with seizures was carried out.

Evaluation of anamnestic data, antenatal, intrapartum risk factors with using statistical methods showed that mothers of newborns (respectively, full-term and premature) with seizures had a high percentage of extragenital diseases (31.8±3.7% χ2 = 15.4, p = 0.009, vs 62.3±5.0% χ2 = 27.2, p1 < 0.001), gynecological disorders (49.1±3.6% χ2 = 37.1 p < 0.001, and 47.0±5.1% χ2 = 9.69 p1 = 0.046), threatened miscarriage (9.1±2.5% χ2 = 11.290 p < 0.001, and 28.5±4.7% χ2 = 14.779 p1 < 0.001), anemia of pregnancy (40.0±3.6% χ2 = 14.9 , p < 0.001 vs 66.4±4.3% χ2 = 18.9, p < 0.001). After EEG examination, we found that in most cases, 78 (30.0%) newborns exhibited polymorphic convulsions, i.e. a combination of different types of convulsions. The atypical convulsions were reported in 64 (24.5%) newborns, with a predominance of preterm infants 61 (40.4%). Clonic seizures were more common in full-term infants (n = 34; 30.9%) and preterm (n = 26; 17.2%). Myoclonic convulsions were found mainly in preterm newborns 21% (13.9%). Tonic convulsions were found in only 5 cases (5.3%). According to neurosonographic data, brain swelling was reported in 83 (31.8%), ventriculomegaly in 44 (16.9%), ventriculitis in 43 (16.5%), intraventricular hemorrhage in 66 (15.3%) newborns of the main group. In the control group, periventricular hemorrhage was observed in 37 (14.2%) newborns. Frequency of these disorders in preterm infants was 18.6% higher than in full-term infants (χ2 = 13.3; p = 0.004). Altered immunological reactivity in newborns with seizures manifested as abnormal cytokine status and significantly elevated pro-inflammatory cytokines (IL-1β, 1.9-fold; IL-6, 3-fold; TNFα 3.3-fold increase) compared with newborns of control group. Increased concentration of pro-inflammatory cytokines in newborns with HIE is associated with maintenance of seizure activity and aggravates further unfavorable neurological outcome. The cerebral disorders and dysfunction of different organs and systems were found to correlate with immune parameters. Hence, the expression of pro-inflammatory cytokines may be used as a screening marker in diagnostics and prediction of neonatal seizures in presence of perinatal hypoxic-ischemic lesions of the central nervous system.

Russian Journal of Immunology. 2022;25(1):55-62
pages 55-62 views
Immunity parameters in adults with measles compared with healthy persons
Toptygina A.P., Andreev Y.Y.
Abstract

Measles is a highly contagious viral infection transmitted by airborne droplets, characterized by fever, intoxication and specific rashes on the skin and mucous membranes. Despite the availability of highly effective vaccines and many years of efforts by the world medical community with active immunization of the world’s population against this infection under the auspices of WHO, measles still remains a serious problem. The aim of this work was to investigate the effect of measles infection in adults upon the wide range of lymphocyte subsets and blood cytokine profile in comparison with healthy controls.

The venous blood samples from 50 adult measles patients aged 20 to 55 years, were taken 6±1 days after the onset of skin rash, being compared with blood samples from 50 healthy adults of similar age group. The 200 μL plasma aliquotes resulting from spontaneous sedimentation of the formed elements in an Eppendorf tube were taken, frozen at -30 °C and used within 3 months for the cytokine profile assays. 15 cytokines were tested by multiplex technique (MagPix, BioRad, USA). Mononuclear cells were isolated by gradient centrifugation and immunophenotyped using four-color staining by means of equipment and reagents from BD Biosciences (USA).

In the group of measles patients, activation of innate immunity was revealed, i.e., the IL-1, IL-6, IL-23, IL-31 cytokines and TNF, which belong to early pro-inflammatory cytokines, were significantly increased. In measles patients, a significant increase in cytokines was found, suggesting active participation of epithelial cells in immune response to the measles virus. They produce danger signals (IL-25 and IL-33), inducing the development of adaptive immunity, activate their protective abilities via IL-17F production, and are involved in repair under the influence of IL-22. Some cells of adaptive immunity are infected with the measles virus and die, others actively respond to the viral infection and proliferate, thus leading to changing ratio of their subsets. Hence, the patients showed a significant decrease in T lymphocytes due to a decrease in CD4+ cells, an increased percentage of cells in “senescent” and “exhaustion” state, a significant decrease in TEMRO subpopulations, both among CD4+ and CD8+ lymphocytes, and an increase in CD8+TCM. The levels of B cell subpopulations (Bm, B1, Breg) in measles patients did not differ from healthy ones, and the level of plasmablasts was significantly increased. The level of CD4+ lymphocyte subpopulations and production of their cytokine markers varied greatly. In the patient group, a shift in the type of immune response towards Th2 and Th17 was found, activation of Tfh and Treg was detected, and increased expression of HLA-DR and CD38 activation markers was found.

In response to measles infection, there are several independent, multidirectional processes observed in the patients. On the one hand, the measles virus attacks epithelial cells of mucous membranes and skin and immunocompetent cells, exerting a cytopathic effect and leading to lymphopenia and selective decrease in various lymphocyte subsets. On the other hand, the measles virus initiates activation of both innate and adaptive immunity, thus causing production of the corresponding cytokines, expression of activation markers, and an increase in effector cell subsets. Better understanding of the immunopathogenesis of measles infection and associated immunosuppression will help us to improve vaccination outcomes against this infection and prevent measles-related mortality.

Russian Journal of Immunology. 2022;25(1):63-72
pages 63-72 views
Functional state of regulatory CD4+T cell pool in HIV/hepatitis C virus coinfected subjects
Saidakova E.V., Korolevskaya L.B., Shmagel K.V.
Abstract

Coinfection with HIV and hepatitis C virus (HCV) leads to development of systemic inflammation associated with increased risk for liver, kidney and cardiovascular diseases, as well as higher mortality from AIDS-associated and non-AIDS-associated illnesses. To a large extent, systemic inflammation is controlled by regulatory T lymphocytes, a subset of CD4+ T cells. While expressing various functional molecules, regulatory CD4+T cells limit functional activity of immunocytes and prevent the development of excessive inflammatory reactions and autoimmune diseases. At the same time, there are no available data in literature concerning the sizes of certain functionally active regulatory CD4+T cell subsets in HIV/HCV coinfected patients. Our aim was to estimate the size of functional pool of the regulatory CD4+T lymphocytes in HIV/ HCV coinfected patients receiving antiretroviral therapy.

Two groups of HIV-positive patients were examined: 1) HIV/HCV coinfected subjects (n = 21); 2) HIV mono-infected patients (n = 22). The control group included voluntary blood donors without HIV and HCV infections (n = 23). Regulatory CD4+T lymphocytes were identified by multicolor flow cytometry based on the expression of the following markers: CD3, CD4, CD25, CD127, and FoxP3. Functional subsets of regulatory CD4+T cells were discerned by the expression of CD39, GARP, LAP, and CD71 molecules. Relative and absolute counts of suppressor CD4+T lymphocytes were calculated for each subset. TGF-β1 concentrations in blood plasma were determined with ELISA technique.

Absolute counts of regulatory CD4+T lymphocytes in peripheral blood of HIV/HCV coinfected patients proved to be twice lower than in healthy subjects, while being not accompanied by a decrease in relative frequency of these cells. Despite their deficiency, the number of functionally active CD39-positive,

GARP/LAP-positive, and CD71-positive suppressor cells in HIV/HCV coinfected persons remained at the level found in HIV-monoinfected and healthy people. The frequency of functionally active regulatory CD4+T lymphocytes was increased in HIV/HCV coinfected patients compared with HIV-monoinfected (CD39+, GARP+LAP+) and healthy (CD39+, GARP+LAP+, CD71+) subjects.

In HIV/HCV coinfected patients receiving antiretroviral therapy, the pool of regulatory CD4+T lymphocytes is rich in cells possessing high suppressive capacity. However, the absolute number of functionally active regulatory CD4+T cells remain at the level corresponding to healthy individuals, thus, apparently, is not sufficient to control the systemic inflammation developing in HIV/HCV coinfection.

Russian Journal of Immunology. 2022;25(1):73-82
pages 73-82 views
Association between polymorphic eNOS gene markers and risk of primary open-angle glaucoma in the Perm Region population
Gavrilova T.V., Kinkulkina A.R., Avagyan H.S., Svitich O.A.
Abstract

Glaucoma is widely known to have a progressive course and occupy a leading place among the causes of vision loss and blindness. Increased intraocular pressure is the key harmful factor among the causes of glaucoma occurrence. In some cases, however, the progressive disease is also observed at normal values of ophthalmic tonus. Early diagnosis of glaucoma will allow for timely therapy, which in turn will reduce the risk of complications and prevent neuroopticopathy progression. According to the literature data, the pathogenesis of primary open-angle glaucoma is associated with nitric oxide (NO), due to imbalance between endothelium-produced vasoconstrictors and vasodilators, especially, endotelin-1 and nitric oxide. Decreased NO level combined with endotelin-1 hyperproduction is associated with development and progression of a number of ocular disorders including glaucomatous atrophy of the optic nerve. Since nitric oxide is produced by endothelial NO-synthase (eNOS), one may assume that eNOS is involved in pathogenesis of neurodegenerative changes in primary open-angle glaucoma. However, despite numerous studies on the pathogenesis of glaucoma, the distinct factors of innate immune response remain poorly studied. The purpose of the present study was a search for association between polymorphic markers (C774T, T786C, Glu298Asp) of the eNOS gene and the risk of primary open-angle glaucoma among the Perm Region residents.

Peripheral blood of patients with primary open-angle glaucoma (the main group) and cataract without glaucoma (a comparison group) was used as initial biomaterial. In comparison group, arterial hypertension was most often encountered as concomitant pathology. Genomic DNA was first isolated from the blood samples, followed by rt-PCR using reagent kits for determining C774T, T786C, Glu298Asp polymorphic markers in the eNOS gene.

The prevalence of polymorphic variants of the innate immunity genes T786C, C774T and Glu298Asp of the eNOS gene was analyzed in patients with primary open-angle glaucoma. There were no significant differences in the distribution of genotypes and alleles of eNOS gene for the C774T and Glu298Asp polymorphic markers. An increased frequency of homozygous TT genotype was found, along with decreased occurrence of C allele at the polymorphic T786C locus of the eNOS gene, as well as a trend for decreased frequency of the TC and CC genotypes. Arterial hypertension potentiated the negative effect of increased intraocular pressure upon the glaucoma-associated optic neuropathy. Conclusions. The studied changes in genotypes and allelic frequencies of eNOS gene may be regarded as risk factors that increase probability of the primary open-angle glaucoma and predict severity of the disease.

Russian Journal of Immunology. 2022;25(1):83-92
pages 83-92 views

SHORT COMMUNICATIONS

Killer cell cluster immunity state in adult patients with common variable immunodeficiency
Prokopovich S. ., Novikova I.A.
Abstract

The subpopulation spectrum of killer cluster lymphocytes in peripheral blood was assessed by flow cytometry in combination, along with analysis of clinical manifestations in 30 adult patients (12 males and 18 females, mean age 37.5±12.3 years) diagnosed with common variable immunodeficiency (CVID). All the patients were observed at the Department of Immunopathology and Allergology at the State Institution “Republican Scientific and Practical Center of Radiation Medicine and Human Ecology” (Gomel, Republic of Belarus). The diagnosis was based on clinical and laboratory criteria developed by the European Society for Immunodeficiencies, using Common Variable Immunodeficiency Diagnostic Criteria, 2020. The patients were examined in the apparent absence of infectious inflammatory disease, prior to monthly immunoglobulin injections. The control group consisted of 30 healthy subjects, comparable in age and sex with the patients’ cohort, free of clinical and laboratory signs of immunological insufficiency. The patients with CVID had a reduced content of NK cells (CD3-CD16+CD56+) and CD3-CD8+ lymphocytes in peripheral blood (p% = 0.009, rabs = 0.03 and p%, abs < 0.001 respectively), along with increase of T cytotoxic cells and NKT lymphocytes (CD3+CD8+; p% = 0.02, rabs = 0.009 and CD3+CD16+CD56+; p%, < 0.001, rabs = 0.004, respectively). Severe NK cell lymphopenia showed inverse correlation with the numbers of T cyclers (rs% = -0.545, p = 0.03), activated T cytotoxic lymphocytes (CD3+CD8+CD38+; rs% = -0.38, p = 0.04), and directly correlated with CD3-CD8+ cell counts (rs% = 0.481, p = 0.008). We also revealed a correlation between the parameters of killer lymphocyte cluster (CD3-CD16+CD56+, CD3-CD8+, CD3+CD16+CD56+) and severity of clinical manifestations in CVID patients. The most pronounced changes in the killer cell subpopulations were observed in patients with a combined clinical phenotype “infection syndrome + autoimmune syndrome” and “infection syndrome + autoimmune syndrome + enteropathy”. Thus, the marked changes of killer cell subpopulations manifesting as decreased counts of NK cells and CD3-CD8+ lymphocytes, along with increased NKT lymphocytes and T killer numbers are associated with more severe clinical phenotypes of CVID and, above all, with development of autoimmune disorders.

Russian Journal of Immunology. 2022;25(1):93-98
pages 93-98 views
Oil-producing enterprise
Nikonoshina N.A., Dolgikh O.V., Zaitseva N.V.
Abstract

Arterial hypertension is an urgent health problem worldwide causing an increase in temporary and permanent disability, invalidity and mortality due to cardiovascular diseases. Researchers recognize the multifactorial nature of arterial hypertension, but environmental factors are of particular potential importance. The working conditions at oil production enterprises are characterized by a more pronounced influence of these factors which may predispose for early development of disadaptation disorders, functional changes in immune and humoral regulation, and, finally, for increased risk of cardiovascular diseases in people engaged in oil production. The aim of the present work was to study the features of immunity and humoral risk factors of arterial hypertension in hypertensive employees at an oil-producing enterprise. To this purpose, a comparative analysis of lymphocyte subpopulations (CD3+CD4+, CD3+CD25+), markers of apoptosis (CD3+CD95+, TNFR, p53, Bax, Annexin V-FITC+7AAD), phagocytic activity of leukocytes (absolute phagocytosis index), and the levels of vascular humoral factors (nitric oxide and homocysteine) was performed in employees of an oil production enterprise exposed to adverse production factors. The observational group consisted of employees with established episodes of increased blood pressure. A comparison group consisted of individuals without clinical manifestations of cardiovascular disease. As a result of the clinical and laboratory examination of employees at the oil-producing enterprise with arterial hypertension, some functional changes in immune regulation were revealed. This group was characterized by a significantly (p < 0.05) decreased CD3+CD4+, and CD3+CD25+ lymphocyte contents, along with increased levels of regulatory CD127 lymphocytes against the comparison group (p < 0.05). The workers at an oil production enterprise with arterial hypertension are characterized by decreased (p < 0.05) phagocytic activity of peripheral blood leukocytes using the criteria of absolute phagocytosis. We found some signs of inhibited lymphocyte apoptosis (p < 0.05), i.e., a decrease in CD95+, TNFR, and p53 over the background values, as well as increased Bax levels over the comparison group (p < 0.05). However, the content of TNFR and p53 significantly (p < 0.05) exceeded the reference level, regardless of previous arterial hypertension episodes. Development of the high blood pressure episodes among the employees at oi-producing plant showed a significant association (p < 0.05) with elevated levels of homocysteine and nitric oxide concentrations which are known to induce endothelial dysfunction, atherogenesis and, hence, a persistent increase in blood pressure.

Russian Journal of Immunology. 2022;25(1):99-104
pages 99-104 views


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