Nurana Nuralieva

Ministry of Health of the Russian Federation

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ЕА

Е. А. Трошина

Ministry of Health of the Russian Federation

M. Yu. Yukina

Ministry of Health of the Russian Federation

Marina Yukina

Ministry of Health of the Russian Federation

Elena Savvateeva

Engelhardt Institute of Molecular Biology

НМ

Н. М. Платонова

Endocrinology Research Center

Dmitry Gryadunov

Engelhardt Institute of Molecular Biology

ГА

Г. А. Мельниченко

Endocrinology Research Center

НГ

Н. Г. Мокрышева

Endocrinology Research Center

M.Yu. Yukina

Endocrinology Research Center

O. Yu. Rebrova

Pirogov Russian National Research Medical University

Cooperative Institutions

Endocrinology Research Center

Ministry of Health of the Russian Federation

Faculdades Guarulhos

Sechenov University

Lomonosov Moscow State University

National Medical Research Center of Cardiology

Pirogov Russian National Research Medical University

Russian Academy of Sciences

State Research Center for Dermatovenereology and Cosmetology

Engelhardt Institute of Molecular Biology

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Association of the CT genotype of the polymorphic marker rs12979860 of the IL28B gene with autoimmune adrenal insufficiency

Endocrine Abstracts (2024)

Nurana Nuralieva Marina Yukina Ekaterina Meremyanina Е. А. Трошина О. А. Свитич

10.1530/endoabs.104.p2

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ГЕНЕТИЧЕСКИЕ ПРЕДИКТОРЫ ПЕРВИЧНОЙ НАДПОЧЕЧНИКОВОЙ НЕДОСТАТОЧНОСТИ АУТОИММУННОГО ГЕНЕЗА

Nurana Nuralieva М Ю Юкина Е. А. Meremianina Е. А. Трошина О. А. Свитич

Аутоиммунная надпочечниковая недостаточность (АНН) часто является компонентом аутоиммунных полигландулярных синдромов (АПС). АПС 1 типа обусловлен мутацией гена аутоиммунного регулятора AIRE, а предрасположенность к АПС 2 типа и изолированной АНН определяется вариантами генов системы HLA. Не исключается, что в модулировании риска изолированной АНН и АНН в рамках АПС 2 типа, а также в фенотипической вариабельности АПС 1 типа играют роль варианты генов, кодирующих toll-подобные рецепторы (TLR2 и TLR9) и интерферон-λ (IL28B), которые участвуют в иммунном ответе и ассоциированы с рядом других аутоиммунных заболеваний. ЦЕЛЬ: выявить ассоциации полиморфных маркеров в генах TLR9, IL28B, TLR2 с наличием АНН. МАТЕРИАЛЫ И МЕТОДЫ: включено n=63 пациента с АНН: n=54 – с изолированной АНН и АНН в рамках АПС 2 типа (группа 1а); n=9 – с АПС 1 типа (группа 1b); и n=32 условно здоровых лиц (группа 2). Участникам выполнен анализ полиморфных маркеров в генах IL28B (rs12979860 и rs8099917), TLR9 (rs5743836 и rs352140) и TLR2 (rs5743708) методом полимеразной цепной реакции в реальном времени. РЕЗУЛЬТАТЫ: В группе 1 по сравнению с группой 2 выявлено статистически значимое преобладание генотипа СТ полиморфного маркера rs12979860 гена IL28B (р=0,010), а также аллеля Т полиморфизма rs5743836 гена TLR9 (р=0,032). Напротив, генотип СС полиморфизма rs12979860 гена IL28B (р=0,025) и аллель С полиморфизма rs5743836 гена TLR9 (р=0,032) чаще встречались в группе 2, чем в группе 1. При сравни- тельном анализе распределения частот гаплотипов по двум локусам гена IL28B (rs8099917 и rs12979860) обнаружено, что CCTT встречается значительно чаще в группе 2, по сравнению с группой 1 (р=0,024). При сравнении групп 1а и 2 статистическая значимость сохранялась только в отношении частот генотипа СТ полиморфизма rs12979860 гена IL28B (р=0,024) и аллелей Т и С полиморфизма rs5743836 гена TLR9 (р=0,044). В группе 1b по сравнению с группой 2 наблюдалось преобладание генотипа СТ полиморфного маркера rs12979860 гена IL28B (р=0,032) и гаплотипа CTTT по двум локусам гена IL28B: rs8099917 и rs12979860 (р=0,020). ВЫВОДЫ: пациенты с АНН как изолированной, так и в составе АПС 1 и 2 типов отличаются от условно здоровых лиц более частым носительством генотипа СТ полиморфного маркера rs12979860 гена IL28B. Аллель Т полиморфизма rs5743836 гена TLR9 является прогностическим маркером, повышающим ве- роятность развития АНН, тогда как генотип СС по полиморфному локусу rs12979860 гена IL28B, гаплотип CCTT по двум локусам гена IL28B (rs8099917 и rs12979860) и аллель С полиморфизма rs5743836 гена TLR9 – выполняют протективную роль при данном заболевании.

TLR9

10.14341/cong23-26.05.23-53

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Nondiabetic hypoglycemia: the role of psycho-neurological care in primary diagnosis

Endocrine Abstracts (2023)

M. Yu. Yukina Nurana Nuralieva Е. А. Трошина

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

10.1530/endoabs.90.ep1116

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Trio-Based Exome Sequencing and High-Resolution HLA Typing in Families of Patients with Autoimmune Adrenal Insufficiency and Autoimmune Polyglandular Syndrome

Anastasiia A. Buianova M. Yu. Yukina Valery Cheranev Oleg N. Suchalko Anna Shmitko

Trio-based exome sequencing and high-resolution HLA typing were employed to analyze three patients with autoimmune adrenal insufficiency (AAI), including those with autoimmune polyglandular syndrome (APS) type 2, as well as their parents. Benign or likely benign variants of the AIRE gene were identified in all participants of the study. These variants, coupled with clinical data and the results of antibody studies to type I interferons, helped to exclude APS-1. Patients with APS-2, in contrast to patient with AAI, inherited distinct variants of unknown significance in the CLEC16A gene, which is associated with autoimmune diseases including AAI. Various risk alleles in other genes associated with autoimmunity were identified in all patients. HLA typing of second class loci revealed alleles related to APS types 2, 3, and 4. Nevertheless, the frequencies of the haplotypes identified are substantial in the healthy Russian population, precluding from regarding these alleles as genetic determinants linked to APS development. Immunological examination can detect antibody carriers and predict the risk of autoimmune disease development. In the future, to identify genetic predictors of autoimmune endocrinopathies, it is recommended to analyze the whole genome of patients and their relatives, examining clinically relevant variants in non-coding regions.

Exome

10.20944/preprints202311.1812.v1

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The autoimmune IgG4 -associated endocrine pathology

Obesity and metabolism (2017)

M. Yu. Yukina Е. А. Трошина Н. М. Платонова Nurana Nuralieva

Immunoglobulin G4-associated diseases (IgG4-AD) arethe group of chronic progressive autoimmune fibro-inflammatory pathology of various organs and tissues, characterized by their enlargement and abundant infiltration of immunoglobulin G4-positive plasma cells, as well as an increase in the level of serum immunoglobulin G4 (IgG4).In most patients, the disease is characterized by a mild course.However, there is evidence of a high incidence of malignancies in patients with IgG4-AD.Among endocrine IgG4-associated pathologies, pancreatitis with outcome in diabetes mellitus, hypophysitis and thyroiditis are described. Laboratory examination usually reveals an increased level of IgG4. However, the concentration of IgG4 could not be used as the only diagnostic criterion.The possibility of plasmablastsdetermining as a marker of the disease is discussed.Among the imaging techniques CT, MRI and 18F-FDG-PET/CT are used.However, the most informative method of diagnosis is biopsy. Randomized clinical trials to determine clear recommendations for the treatment of IgG4-AD were not conducted.In most cases, glucocorticoids are prescribed, and immunosuppressive therapy is sometimes used.According to the results of recent studies, the genetically engineered drug rituximab is relatively effective in inducing remission of the disease.Given the high recurrence rate and the risk of malignancy, patients with IgG4-AD require careful long-term follow-up. Thus, the review describes the clinical manifestations of IgG4-AD, examines the possibilities of their diagnosis and presents the existing methods of treatment.However, given the fact that IgG4-AD became a separate group of autoimmune pathology less than 20 years ago, there are insufficient data on these diseases. Researches related to epidemiology, pathophysiology, diagnosis and effective treatment of IgG4-AD are actual.

Autoimmune Pancreatitis

IgG4-Related Disease

Hypophysitis

10.14341/omet2017343-47

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Microarray-based detection of antibodies against SARS-CoV-2 proteins, common respiratory viruses and type I interferons

medRxiv (Cold Spring Harbor Laboratory) (2021)

Elena Savvateeva М. А. Филиппова Vladimir T. Valuev-Elliston Nurana Nuralieva M. Yu. Yukina

Abstract A microarray-based assay to detect IgG and IgM antibodies against betacoronaviruses (SARS-CoV-2, SARS, MERS, OC43, and HKU1), other respiratory viruses and type I interferons (IFN-Is) was developed. This multiplex assay was applied to track antibody cross-reactivity due to previous contact with similar viruses and to identify antibodies against IFN-Is as the markers for severe COVID-19. In total, 278 serum samples from convalescent plasma donors, COVID-19 patients in the intensive care unit (ICU) and patients who recovered from mild/moderate COVID-19, vaccine recipients, prepandemic and pandemic patients with autoimmune endocrine disorders, and a heterogeneous prepandemic cohort including healthy individuals and chronically ill patients were analyzed. The anti-SARS-CoV-2 microarray results agreed well with the ELISA results. Regarding ICU patients, autoantibodies against IFN-Is were detected in 10.5% of samples, and 10.5% of samples were found to simultaneously contain IgM antibodies against more than two different viruses. Cross-reactivity between IgG against the SARS-CoV-2 nucleocapsid and IgG against the OC43 and HKU1 spike proteins was observed, resulting in positive signals for the SARS-CoV-2 nucleocapsid in prepandemic samples from patients with autoimmune endocrine disorders. The presence of IgG against the SARS-CoV-2 nucleocapsid in the absence of IgG against the SARS-CoV-2 spike RBD should be interpreted with caution.

Coronavirus

Multiplex

10.1101/2021.12.13.21267509

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Continuous glucose monitoring during the prolonged fast test for the diagnosis of hypoglycemic diseases: primary data analysis

Endocrine Abstracts (2019)

Marina Yukina Nurana Nuralieva Е. А. Трошина

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

10.1530/endoabs.63.p54

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