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1.
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    In HIV-infected immunological non-responders, hepatitis C virus eradication contributes to incomplete normalization of systemic inflammation, but does not lead to rapid CD4+ T-cell count recovery / E. V. Saidakova, L. B. Korolevskaya, N. G. Shmagel [et al.] // Doklady Biochemistry and Biophysics. - 2023. - Vol. 512. - P274–278
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
HIV INFECTIONS -- HEPATITIS C -- IMMUNOLOGICAL NON-RESPONSE
Аннотация: In HIV-positive individuals taking antiretroviral therapy, coinfection with hepatitis C virus (HCV) increases systemic inflammation, which interferes with the CD4+ T-cells regeneration. This study evaluated the effect of HCV eradication on systemic inflammation and CD4+ T-cell regeneration in patients who gave poor response to antiretroviral therapy, the so-called “immunological non-responders” (INRs). HIV-infected patients who received a course of direct-acting antivirals for treating hepatitis C were examined. The control groups included HIV/HCV-coinfected INRs and relatively healthy volunteers. It was established for the first time that HCV eradication is not accompanied by a complete suppression of systemic inflammation, but improves the T-cell pool composition: in INRs, the blood CD4+/CD8+ T-lymphocyte ratio increases and approaches those of healthy individuals. Apparently, in INRs treated for hepatitis C, the immune system recovery takes time and may be incomplete.

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2.
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    Role of proinflammatory cytokines in hashimoto's thyroiditis associated with psychiatric disorders / P. A. Sobolevskaya, A. N. Gvozdeckii, I. V. Kudryavtsev [и др.] // Medical Immunology. - 2023. - Vol. 25, № 5. - С. 1247-1252
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Аннотация: Mental disorders often accompany autoimmune diseases, for example, since 1949 it has been known about “myxedematous madness”, a psychosis caused by hypothyroidism. The most common cause of hypothyroidism is Hashimoto's autoimmune thyroiditis. It is also known about another neuropsychiatric disorder associated with autoimmune thyroiditis, Hashimoto's encephalopathy. It is a severe dysfunction of the central nervous system, the pathogenesis of which is not associated with hormonal disorders. Cytokines are regulators and participants of inflammation, including autoimmune. Certainly, when we are talking about high concentrations cytokines, we mean systemic inflammation. The minimal or mediocre fluctuations in cytokines within the ranges that are characteristic of healthy status or normergic acute phase response in disease cannot be interpreted from the point of view of binary endocrinological logic. In the CNS, cytokines are able to influence on the neuroendocrine control of systemically regulated functions. It is also important that glial cells (astroglia, microglia) are capable of producing a number of cytokines and can affect neurons and develop behavioral changes. In addition, the ability of a number of cytokines outside the CNS itself to act on vagal afferents and through them to convey information to the CNS, affecting its state and functions, has been proven. It is reasonable to assume that minimal fluctuations in cytokine levels may also affect the state and function of the CNS. The aim of the study was to investigate the levels of cytokines in patients with thyroiditis; in patients with thyroiditis associated with mental disorders; in a group of healthy individuals; and evaluate the effect of cytokine levels on clinical manifestations. In the group of patients with thyroiditis and mental disorders, the levels of CCL20/MIP3α, IL-13, IL-2, IL-27, IL-5 were significantly higher than in other groups. At the same time, no positive correlation was found between the clinical manifestations of mental disorders and the levels of cytokines. A positive correlation was found between the levels of some cytokines and free triiodothyronine, as well as the level of antithyroid antibodies. Mental disorders associated with autoimmune thyroiditis may be associated with changes in the cytokine profile and result from neuroinflammation.

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3.
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    Alpha-fetoprotein as a factor of differentiation and functional activity of myeloid-derived suppressor cells / K. Yu. Shardina, S. A. Zamorina, V. P. Timganova [et al.] // Bulletin of experimental biology and medicine. - 2023. - Vol. 175. - P535–543
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Аннотация: We studied the role of alpha-fetoprotein (AFP) in regulation of differentiation and functional activity of human myeloid-derived suppressor cells (MDSC) in vitro. To obtain MDSC, CD11b+ cells were isolated from the peripheral blood of healthy donors followed by cytokine induction (IL-1β+GM-CSF) into the MDSC phenotype. The cell functions were assessed by the expression of indoleamine 2,3-dioxygenase (IDO) and arginase-1 (Arg1) and cytokine profile of the cell cultures. Native AFP did not affect the total number of MDSC and the percentage of polymorphonuclear MDSC (PMN-MDSC), but increased the number of monocytic MDSC (M-MDSC). AFP did not change the expression of Arg1, but in low concentrations (10 and 50 U/ml) increased the number of IDO-containing cells. AFP modulated the cytokine profile of CD11b+ cells: it reliably decreased the level of IL-19 (50 and100 U/ml) and showed a tendency to decrease the levels of IL-34, MMP-2, sCD163, CHI3L1, OPN and to increase the levels of IL-29, IL-32, APRIL, PTX3, and sTNF-R1. Thus, we have demonstrated a regulatory effect of native AFP at the level of MDSC generated from CD11b+ cells under conditions of cytokine induction in vitro.

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4.
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    Th17-lymphocytes and their cytokines in pathogenesis of autoimmune thyroiditis, aсcompanied by psychiatric disorders / P. A. Sobolevskaya, A. N. Gvozdeckii, I. V. Kudryavtsev [et al.] // 9th International Congress of Pathophysiology and 5th Congress of Physiological Sciences of Serbia with International Participation. Final Program and Abstract Book. - Kragujevac, 2023. - P50
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
AUTOIMMUNE THYROIDITIS -- PSYCHIATRIC DISORDERS -- LYMPHOCYTES

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5.
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   I-34

   
    Identification of the immune subtype among muscle-invasive bladder cancer patients by multiple datasets / K. Shinwari, Z. Chen, Z. Liu Guojun [et al.] // Acta Medica Indonesiana. - 2022. - Vol. 54, № 1. - P62-71
ББК 61
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
MOLECULAR SUBTYPE -- IMMUNOTHERAPY -- MIBC
Аннотация: Background: Immunotherapies including PD-1/PD-L1 antibodies have been approved for the treatment of Muscle-invasive Bladder Cancer (MIBC) patients. However, immunotherapies could only be beneficial for about 20% MIBC patients. Thus, identification of the immune subtype is becoming increasingly important. This study aimed to explore the immune subtype by analyzing the gene expression profiles. Methods: A total of 6 datasets including (GSE13507, GSE31684, GSE32548, GSE32894, GSE69795, and TCGA-BLCA) were downloaded. The gene expression profiles from different datasets were combined since the batch effects were removed. We performed unsupervised clustering analysis to identify the immune subtype by the combined gene expression profiles. The tumor-infiltration levels of 22 immune cells, immune scores, and tumor purity were calculated, and the survival analysis was performed to investigate the prognosis difference between immune subtypes. The enriched pathways for each immune subtype were obtained. Results: We identified four novel immune subtypes (referred to S1, S2, S3, and S4) among MIBC patients. We found that S1 was enriched in immune scores had the best prognosis. In contrast, S3 was poor in immune scores and had the worst prognosis. Subtype S1, S2, S3, and S4 were enriched in immune-related pathways, extracellular matrix-related pathways, metabolism-related pathways, and cancer-related pathways, respectively. Conclusion: The current study suggests that the immune subtypes based on gene expression profiles could contribute to select the appropriate MIBC patient for immunotherapies.

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6.
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    Novel disease-associated missense single-nucleotide polymorphisms variants predication by algorithms tools and molecular dynamics simulation of human TCIRG1 gene causing congenital neutropenia and osteopetrosis / K. Shinwari, H. Rehman, H. Liu Guojun [et al.] // Frontiers in Molecular Biosciences. - 2022. - Vol. 9. - Ст. 879875
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Аннотация: T Cell Immune Regulator 1, ATPase H + Transporting V0 Subunit A3 (TCIRG1 gene provides instructions for making one part, the a3 subunit, of a large protein complex known as a vacuolar H + -ATPase (V-ATPase). V-ATPases are a group of similar complexes that act as pumps to move positively charged hydrogen atoms (protons) across membranes. Single amino acid changes in highly conserved areas of the TCIRG1 protein have been linked to autosomal recessive osteopetrosis and severe congenital neutropenia. We used multiple computational approaches to classify disease-prone single nucleotide polymorphisms (SNPs) in TCIRG1. We used molecular dynamics analysis to identify the deleterious nsSNPs, build mutant protein structures, and assess the impact of mutation. Our results show that fifteen nsSNPs (rs199902030, rs200149541, rs372499913, rs267605221, rs374941368, rs375717418, rs80008675, rs149792489, rs116675104, rs121908250, rs121908251, rs121908251, rs149792489 and rs116675104) variants are likely to be highly deleterious mutations as by incorporating them into wild protein they destabilize the wild protein structure and function. They are also located in the V-ATPase I domain, which may destabilize the structure and impair TCIRG1 protein activation, as well as reduce its ATPase effectiveness. These mutants have not yet been identified in patients suffering from CN and osteopetrosis while (G405R, R444L, and D517N) reported in our study are already associated with osteopetrosis. Mutation V52L reported in our study was identified in a patient suspected for CN. Finally, these mutants can help to further understand the broad pool of illness susceptibilities associated with TCIRG1 catalytic kinase domain activation and aid in the development of an effective treatment for associated diseases.

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7.
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    Checking gene expression profile associated with IRF7 and UNC93B deficient patient peripheral blood mononuclear cells infected with pH1N1 influenza virus / K. Shinwari, G. Liu, M. A. Bolkov [et al.] // AIP Conference Proceedings. - 2022. - Vol. 2390, № 1. - Ст. 030089
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
VIRUSES -- MICROARRAYS -- GENOMICS
Аннотация: An innate immune defect is a defect in the innate immune response that reduces the response to infection, this can occurs in genes important for activation regulation and proliferation of the innate immune cells or pathways important for the function of innate immunity. The purpose of this study was to identify novel biomarkers of interferon Receptor 7 through bioinformatics analysis and elucidate the possible molecular mechanism. The GSE 66486 datasets containing microarray data from IRF7 and UNC93B patients and healthy controls were downloaded from the GEO database and analyzed by the GEO2R web tool to obtain different expressed genes (DEGs). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI), and Biological Networks Gene Oncology tool (BiNGO) were then performed to elucidate the molecular mechanism of IRF7. A total of 490 DEGs were identified, of which 14 were hub genes, and involved in ribosome biogenesis, rRNA processing, gene expression, mRNA processing, nuclear lumen, intracellular non-membrane-bounded organelle, nucleoplasm, small-subunit processome, antigen processing and presentation pathway, and ribosome biogenesis in eukaryotes. Antigen processing and presentation pathway, and ribosome biogenesis in eukaryotes possibly form the basis of IRF7 or UNC93B disorders, while our study provides a list of genes and pathways that are disrupted in IRF7/UNC93B, which has the potential to be used in the clinic for diagnosis and targeted therapy of such disorders in future.

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8.
Инвентарный номер: нет.
   

   
    Defining muscle-invasive bladder cancer immunotypes by introducing tumor mutation burden, CD8+ T cells, and molecular subtypes / Zihao Chen, Guojun Liu, Guoqing Liu [et al.]. - https://doi.org/10.1186/s41065-020-00165-7 // Hereditas. - 2021. - Vol. 158, № 1. - 12 p
Кл.слова (ненормированные):
CD8+ T CELLS -- MOLECULAR SUBTYPE -- IMMUNOTHERAPY
Аннотация: Immunotherapy, especially anti-PD-1, is becoming a pillar of modern muscle-invasive bladder cancer (MIBC) treatment. However, the objective response rates (ORR) are relatively low due to the lack of precise biomarkers to select patients. Herein, the molecular subtype, tumor mutation burden (TMB), and CD8+ T cells were calculated by the gene expression and mutation profiles of MIBC patients. MIBC immunotypes were constructed using clustering analysis based on tumor mutation burden, CD8+ T cells, and molecular subtypes. Mutated genes, enriched functional KEGG pathways and GO terms, and co-expressed network-specific hub genes have been identified. We demonstrated that ORR of immunotype A patients identified by molecular subtype, CD8+ T cells, and TMB is about 36% predictable. PIK3CA, RB1, FGFR3, KMT2C, MACF1, RYR2, and EP300 are differentially mutated among three immunotypes. Pathways such as ECM-receptor interaction, PI3K-Akt signaling pathway, and TGF-beta signaling pathway are top-ranked in enrichment analysis. Low expression of ACTA2 was associated with the MIBC survival benefit. The current study constructs a model that could identify suitable MIBC patients for immunotherapy, and it is an important step forward to the personalized treatment of bladder cancers.

\\\\Expert2\\NBO\\Электрон. библиотека (Отеч.периодика)\\Черешнев В. А\\Hereditas. - 2021. - Vol. 158, № 1.pdf
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9.
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    Antinuclear autoantibodies in healthy individuals: autoimmunity is not a synonym of autoimmune disease : doi.org/10.3390/antib10010009 / I. A. Pashnina, I. M. Krivolapova, T. V. Fedotkina [et al.] // Antibodies. - 2021. - Vol. 10, № 1. - Ст. 9
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Аннотация: Incidence of autoimmune diseases increases. Antinuclear antibodies (ANA) testing is a critical tool for their diagnosis. However, ANA prevalence in health increased over last decades, especially among young people. ANA in health occur in low concentrations, with prevalence up to 50% in some populations, which demands a cutoff revision. The review deals with origin and probable physiological or compensatory function of ANA in health, according to the concept of immunological clearance, theory of autoimmune regulation of cell functions and the concept of functional autoantibodies. Considering ANA titers ≤1:320 as a serological marker of autoimmune diseases seems inappropriate. The role of anti-DFS70/LEDGFp75 autoantibodies is highlighted as possible anti-risk biomarker for autoimmune rheumatic disorders. ANA prevalence in health is different in various regions due to several underlying causes discussed in the review, all influencing in additive combinations according to the concept of the mosaic of autoimmunity. Not only titer, but the HEp-2 IFA staining patterns, like AC-2, is also important. Accepting autoantibodies as a kind of bioregulators, not only upper, but also lower borders of their normal range should be determined. Not only their excess, but also lack of them or “autoimmunodeficiency” could be a reason of disorders.

\\\\Expert2\\NBO\\Электрон. библиотека (Отеч.периодика)\\Черешнев В. А\\Antibodies. - 2021. - Vol. 10, № 1. - Ст. 9.pdf
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10.
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    Pathogenesis of autoimmune male infertility: Juxtacrine, paracrine and endocrine deregulation / V. A. Chereshnev, S. V. Pichugova, Y. B. Beikin [et al.] // Pathophysiology. - 2021. - Vol. 28. - P471-486

\\\\nas3\\Nbo\\Электрон. библиотека (Отеч.периодика)\\Черешнев В. А\\Pathophysiology. - 2021. - Vol. 28. - С. 1-17.pdf
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