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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">pediatricjournal</journal-id><journal-title-group><journal-title xml:lang="ru">Архив педиатрии и детской хирургии</journal-title><trans-title-group xml:lang="en"><trans-title>Archives of Pediatrics and Pediatric Surgery</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2949-4664</issn><issn pub-type="epub">3033-6783</issn><publisher><publisher-name>НИКИ детства Минздрава Московской области</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.66825/2949-4664-apps-3-3-81-88</article-id><article-id custom-type="elpub" pub-id-type="custom">pediatricjournal-235</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОР ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>LITERATURE REVIEW</subject></subj-group></article-categories><title-group><article-title>TRAIL-рецепторы в патогенезе крапивницы: анализ современных данных</article-title><trans-title-group xml:lang="en"><trans-title>TRAIL receptors in the pathogenesis of urticaria: Analysis of current data</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0383-5006</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Красилова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Krasilova</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Красилова Елена Владимировна, к. м. н., доцент кафедры клинической иммунологии с курсом последипломного образования</p><p>ул. Бакинская, д. 121, г. Астрахань, 414000</p></bio><bio xml:lang="en"><p>Elena V. Krasilova, Cand. Sci. (Med.), Associate Professor, Department of Clinical Immunology with a Postgraduate Course </p><p>121 Bakinskaya St., Astrakhan, 414000</p></bio><email xlink:type="simple">el25kv@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-4168-4851</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Башкина</surname><given-names>О. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Bashkina</surname><given-names>O. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Башкина Ольга Александровна, д. м. н., заведующий кафедрой факультетской педиатрии</p><p>ул. Бакинская, д. 121, г. Астрахань, 414000</p></bio><bio xml:lang="en"><p>Olga A. Bashkina, Dr. Sci. (Med.), Head of Department of Faculty Pediatrics</p><p>121 Bakinskaya St., Astrakhan, 414000</p></bio><email xlink:type="simple">bashkina1@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8172-2421</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шелепова</surname><given-names>Т. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Shelepova</surname><given-names>T. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Шелепова Татьяна Николаевна, к. м. н., доцент кафедры клинической иммунологии с  курсом последипломного образования</p><p>ул. Бакинская, д. 121, г. Астрахань, 414000</p></bio><bio xml:lang="en"><p>Tatiana N. Shelepova, Cand. Sci. (Med.), Associate Professor, Department of Clinical Immunology with a Postgraduate Course</p><p>121 Bakinskaya St., Astrakhan, 414000</p></bio><email xlink:type="simple">shelepovatn@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6766-079X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Воронина</surname><given-names>Л. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Voronina</surname><given-names>L. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Воронина Людмила Петровна, д. м. н., заведующий кафедрой клинической иммунологии с  курсом последипломного образования</p><p>ул. Бакинская, д. 121, г. Астрахань, 414000</p></bio><bio xml:lang="en"><p>Lyudmila P. Voronina, Dr. Sci. (Med.), Head of Department of Clinical Immunology with a  Postgraduate Course</p><p>121 Bakinskaya St., Astrakhan, 414000</p></bio><email xlink:type="simple">voroninaluda74@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Астраханский государственный медицинский университет» Минздрава России</institution></aff><aff xml:lang="en"><institution>Astrakhan State Medical University</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>26</day><month>12</month><year>2025</year></pub-date><volume>3</volume><issue>3</issue><fpage>81</fpage><lpage>88</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Красилова Е.В., Башкина О.А., Шелепова Т.Н., Воронина Л.П., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Красилова Е.В., Башкина О.А., Шелепова Т.Н., Воронина Л.П.</copyright-holder><copyright-holder xml:lang="en">Krasilova E.V., Bashkina O.A., Shelepova T.N., Voronina L.P.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://journal.nikid.ru/jour/article/view/235">https://journal.nikid.ru/jour/article/view/235</self-uri><abstract><sec><title>Актуальность</title><p>Актуальность. Понимание механизмов хронизации крапивницы остается ключевой проблемой клинической иммунологии. Нарушение апоптоза через систему TRAIL/TRAIL-R является перспективным направлением для выявления новых патогенетических мишеней и биомаркеров.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. Проведен аналитический обзор литературы. Осуществлен систематизированный поиск в базах PubMed, Scopus, Web of Science, eLibrary и КиберЛенинка за 2000–2025 гг. Отобрано и проанализировано 97 публикаций, соответствующих критериям включения. Применен метод сравнительного патогенетического анализа.</p></sec><sec><title>Результаты</title><p>Результаты. Установлены принципиальные различия в состоянии системы TRAIL/TRAIL-R при острой и хронической крапивнице (ХК). При острой форме отмечается компенсаторное повышение растворимых рецепторов (sTRAIL-R1/ R2), ограничивающее апоптоз. При ХК формируется патологический дисбаланс: стойкое снижение мембранной экспрессии функциональных рецепторов TRAIL-R1/R2 на иммунных клетках сочетается с повышением их растворимых антагонистических форм. Этот двойной дефект приводит к нарушению клиренса активированных клеток и персистенции воспаления. Параметры системы TRAIL/TRAIL-R обладают высоким диагностическим и прогностическим потенциалом для стратификации пациентов и оценки ответа на терапию.</p></sec><sec><title>Выводы</title><p>Выводы. Дисфункция системы TRAIL/TRAIL-R является значимым патогенетическим звеном хронизации крапивницы. Ее количественные и качественные параметры перспективны в качестве клинических биомаркеров. Для внедрения в практику необходимы стандартизированные многоцентровые исследования, в том числе с учетом возрастных особенностей у детей.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. Elucidation of the mechanisms of urticaria chronification remains a key challenge in clinical immunology. Dysregulation of apoptosis via the TRAIL/TRAIL-R system is a promising direction in identifying new pathogenetic targets and biomarkers.</p></sec><sec><title>Materials and methods</title><p>Materials and methods. An analytical literature review was conducted. A systematic search was performed across the PubMed, Scopus, Web of Science, eLibrary, and CyberLeninka databases for the period from 2000 to 2025. A total of 97 publications meeting the inclusion criteria were selected and analyzed. The method of comparative pathogenetic analysis was applied.</p></sec><sec><title>Results</title><p>Results. Fundamental differences in the state of the TRAIL/ TRAIL-R system between acute and chronic urticaria (CU) were established. In its acute form, a compensatory increase in soluble receptors (sTRAIL-R1/R2) is observed, which limits apoptosis. In CU, a pathological imbalance develops; thus, a persistent decrease in the membrane expression of functional TRAIL-R1/R2 receptors on immune cells is coupled with an increase in their soluble antagonistic forms. This dual defect leads to impaired clearance of activated cells and persistence of inflammation. The parameters of the TRAIL/TRAIL-R system demonstrate a high diagnostic and prognostic potential for patient stratification and assessment of therapy response.</p></sec><sec><title>Conclusions</title><p>Conclusions. Dysfunction of the TRAIL/TRAIL-R system is a significant pathogenetic link in the chronification of urticaria. Its quantitative and qualitative parameters are promising as clinical biomarkers. For implementation into practice, standardized multicenter studies are required, including those considering age-related characteristics in children.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>крапивница</kwd><kwd>хроническая спонтанная крапивница</kwd><kwd>апоптоз</kwd><kwd>программируемая клеточная гибель</kwd><kwd>TRAIL</kwd><kwd>TNFRSF10B</kwd><kwd>DR4</kwd><kwd>DR5</kwd><kwd>растворимые рецепторы</kwd><kwd>биомаркеры</kwd></kwd-group><kwd-group xml:lang="en"><kwd>urticaria</kwd><kwd>chronic spontaneous urticaria</kwd><kwd>apoptosis</kwd><kwd>programmed cell death</kwd><kwd>TRAIL</kwd><kwd>TNFRSF10B</kwd><kwd>DR4</kwd><kwd>DR5</kwd><kwd>soluble receptors</kwd><kwd>biomarkers</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Внешнее финансирование не привлекалось.</funding-statement><funding-statement xml:lang="en">No external funding was attracted.</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Zuberbier T., Abdul Latiff A.H., Abuzakouk M., et al. The international EAACI/GA? LEN/EuroGuiDerm/APAAACI guideline for the definition, classification, diagnosis, and management of urticaria. Allergy. 2022;77(3):734–766. doi: 10.1111/all.15090.</mixed-citation><mixed-citation xml:lang="en">Zuberbier  T., Abdul Latiff  A.H., Abuzakouk  M., et al. The international EAACI/GA? LEN/EuroGuiDerm/APAAACI guideline for the definition, classification, diagnosis, and management of urticaria. Allergy. 2022;77(3):734–766. doi: 10.1111/all.15090.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Kolkhir P., Gimenez-Arnau A.M., Kulthanan K., et al. Autoimmune chronic spontaneous urticaria. Journal of Allergy and Clinical Immunology. 2022;149(6):1819– 1831. doi: 10.1016/j.jaci.2022.04.010.</mixed-citation><mixed-citation xml:lang="en">Kolkhir P., Gimenez-Arnau A.M., Kulthanan K., et al. Autoimmune chronic spontaneous urticaria. Journal of Allergy and Clinical Immunology. 2022;149(6):1819– 1831. doi: 10.1016/j.jaci.2022.04.010.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Лиманский А.В., Коваленко О.Н., Бабак Ю.А. Современные взгляды на иммунные механизмы хронической крапивницы. Иммунология, аллергология и дерматология. 2018;12:36–42.</mixed-citation><mixed-citation xml:lang="en">Limansky A.V., Kovalenko O.N., Babak Yu.A. Modern views on immune mechanisms of chronic urticaria. Immunology, Allergology and Dermatology. 2018;12:36–42. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Лусс Л.В. Роль аллергии и псевдоаллергии в формировании аллергических заболеваний кожи. Аллергология. 2000;3:29–33.</mixed-citation><mixed-citation xml:lang="en">Luss  L.V.  The role of allergy and pseudoallergy in the formation of allergic skin diseases. Allergology. 2000;3:29–33. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Маслова Н.С., Стрекалова Е.И., Проценко Д.М. Молекулярные аспекты патогенеза хронической спонтанной крапивницы. Медицинская наука и практика. 2019;2:45–50.</mixed-citation><mixed-citation xml:lang="en">Maslova N.S., Strekalova E.I., Protsenko D.M. Molecular aspects of the pathogenesis of chronic spontaneous urticaria. Medical Science and Practice. 2019;2:45–50. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Kolkhir P., Church M.K., Weller K., et al. Autoimmune Chronic Spontaneous Urticaria: What We Know and What We Do Not Know. Journal of Allergy and Clinical Immunology. 2017;139(6):1772–1781. doi: 10.1016/j.jaci.2017.04.006.</mixed-citation><mixed-citation xml:lang="en">Kolkhir P., Church M.K., Weller K., et al. Autoimmune Chronic Spontaneous Urticaria: What We Know and What We Do Not Know. Journal of Allergy and Clinical Immunology. 2017;139(6):1772–1781. doi:  10.1016/j.jaci.2017.04.006.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Elmore S. Apoptosis: A Review of Programmed Cell Death. Toxicologic Pathology. 2007;35(4):495–516. doi: 10.1080/01926230701320337.</mixed-citation><mixed-citation xml:lang="en">Elmore  S. Apoptosis: A  Review of Programmed Cell Death. Toxicologic Pathology. 2007;35(4):495–516. doi: 10.1080/01926230701320337.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Strasser A., Jost P.J., Nagata S. The Many Roles of FAS Receptor Signaling in the Immune System. Immunity. 2009;30(2)180–192. doi: 10.1016/j.immuni.2009.01.001.</mixed-citation><mixed-citation xml:lang="en">Strasser A., Jost P.J., Nagata S. The Many Roles of FAS Receptor Signaling in the Immune System. Immunity. 2009;30(2)180–192. doi: 10.1016/j.immuni.2009.01.001.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Johnstone R.W., Frew A.J., Smyth M.J. The TRAIL apoptotic pathway in cancer onset, progression and therapy. Nature Reviews Cancer. 2008;8(10):782–798. doi: 10.1038/nrc2465.</mixed-citation><mixed-citation xml:lang="en">Johnstone  R.W., Frew  A.J., Smyth  M.J.  The TRAIL apoptotic pathway in cancer onset, progression and therapy. Nature Reviews Cancer. 2008;8(10):782–798. doi: 10.1038/nrc2465.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Falschlehner C., Schaefer U., Walczak H. Following TRAIL’s path in the immune system. Immunology. 2009;127(2):145–154. doi: 10.1111/j.1365-2567.2008.03037.x.</mixed-citation><mixed-citation xml:lang="en">Falschlehner  C., Schaefer  U., Walczak  H. Following TRAIL’s path in the immune system. Immunology. 2009; 127(2):145–154. doi: 10.1111/j.1365-2567.2008.03037.x.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Ashkenazi A. Targeting the extrinsic apoptotic pathway in cancer: lessons learned and future directions. The Journal of Clinical Investigation. 2015;125(2):487–489. doi: 10.1172/JCI80420.</mixed-citation><mixed-citation xml:lang="en">Ashkenazi A. Targeting the extrinsic apoptotic pathway in cancer: lessons learned and future directions. The Journal of Clinical Investigation. 2015;125(2):487–489. doi: 10.1172/JCI80420.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Lamhamedi-Cherradi S.E., Zheng S., Tisch R.M., Chen Y.H. Critical roles of tumor necrosis factor-related apoptosis-inducing ligand in type 1 diabetes. Diabetes. 2003;52(9):2274–2278. doi: 10.2337/diabetes.52.9.2274.</mixed-citation><mixed-citation xml:lang="en">Lamhamedi-Cherradi  S.E., Zheng  S., Tisch  R.M., Chen Y.H. Critical roles of tumor necrosis factor-related apoptosis-inducing ligand in type 1 diabetes. Diabetes. 2003;52(9):2274–2278. doi: 10.2337/diabetes.52.9.2274.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Song K., Chen Y., Goke R., et al. Tumor necrosis factorrelated apoptosis-inducing ligand (TRAIL) is an inhibitor of autoimmune inflammation and cell cycle progression. The Journal of Experimental Medicine. 2000;191(7):1095–1104. doi: 10.1084/jem.191.7.1095.</mixed-citation><mixed-citation xml:lang="en">Song K., Chen Y., Goke R., et al. Tumor necrosis factorrelated apoptosis-inducing ligand (TRAIL) is an inhibitor of autoimmune inflammation and cell cycle progression. The Journal of Experimental Medicine. 2000;191(7):1095–1104. doi: 10.1084/jem.191.7.1095.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Kavurma M.M., Tan N.Y., Bennett M.R. Death receptors and their ligands in atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 2008:28(10):1694– 1702. doi: 10.1161/ATVBAHA.108.167353.</mixed-citation><mixed-citation xml:lang="en">Kavurma  M.M., Tan  N.Y., Bennett  M.R.  Death receptors and their ligands in atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 2008:28(10):1694– 1702. doi: 10.1161/ATVBAHA.108.167353.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Cretney E., Takeda K., Yagita H., et al. Increased susceptibility to tumor initiation and metastasis in TNF-related apoptosis-inducing ligand-deficient mice. The Journal of Immunology. 2002;168(3):1356–1361. doi: 10.4049/jimmunol.168.3.1356.</mixed-citation><mixed-citation xml:lang="en">Cretney  E., Takeda  K., Yagita  H., et al. Increased susceptibility to tumor initiation and metastasis in TNF-related apoptosis-inducing ligand-deficient mice. The Journal of Immunology. 2002;168(3):1356–1361. doi: 10.4049/jimmunol.168.3.1356.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Walczak H. Death receptor-ligand systems in cancer, cell death, and inflammation. Cold Spring Harbor Perspectives in Biology. 2013:5(5). a008698. doi: 10.1101/cshperspect.a008698.</mixed-citation><mixed-citation xml:lang="en">Walczak  H.  Death receptor-ligand systems in cancer, cell death, and inflammation. Cold Spring Harbor Perspectives in Biology. 2013;5(5): a008698. doi: 10.1101/cshperspect.a008698.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Chen C., Liu Z., Zhou J., Wu M. Role of TRAIL Receptor Expression in Chronic Urticaria. International Journal of Molecular Sciences. 2019;20(12) Art. 3045. doi: 10.3390/ijms20123045.</mixed-citation><mixed-citation xml:lang="en">Chen  C., Liu  Z., Zhou  J., Wu  M.  Role of TRAIL Receptor Expression in Chronic Urticaria. International Journal of Molecular Sciences. 2019;20(12): Art. 3045. doi: 10.3390/ijms20123045.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Bracken S.J., Abraham S., MacLeod A.S. Autoimmune Theories of Chronic Spontaneous Urticaria. Frontiers in Immunology. 2019;10. Art. 627. doi: 10.3389/fimmu.2019.00627.</mixed-citation><mixed-citation xml:lang="en">Bracken S.J., Abraham S., MacLeod A.S. Autoimmune Theories of Chronic Spontaneous Urticaria. Frontiers in Immunology. 2019;10: Art. 627. doi:  10.3389/fimmu.2019.00627.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Hwang S.J., Kim B.S., Park J.H., Lee K.Y. Clinical significance of soluble TRAIL-R1 and TRAIL-R2 levels in urticaria patients. Clinical &amp; Experimental Allergy. 2021;51(4):485–493. doi: 10.1111/cea.13830.</mixed-citation><mixed-citation xml:lang="en">Hwang  S.J., Kim  B.S., Park  J.H., Lee  K.Y.  Clinical significance of soluble TRAIL-R1 and TRAIL-R2 levels in urticaria patients. Clinical &amp; Experimental Allergy. 2021;51(4):485–493. doi: 10.1111/cea.13830.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Zhao Y., Wang X., Zhang L., Li H. Expression of TRAIL receptors in acute urticaria patients. Journal of Dermatological Science. 2018;91(3):211–218. doi: 10.1016/j.jdermsci.2018.04.014.</mixed-citation><mixed-citation xml:lang="en">Zhao Y., Wang X., Zhang L., Li H. Expression of TRAIL receptors in acute urticaria patients. Journal of Dermatological Science. 2018;91(3):211–218. doi:  10.1016/j. jdermsci.2018.04.014.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">van der Sloot A.M., Tur V., Szegezdi E., et al. Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the DR5 receptor. Proceedings of the National Academy of Sciences. 2006;103(23):8634–8639. doi: 10.1073/pnas.0510187103.</mixed-citation><mixed-citation xml:lang="en">van der Sloot A.M., Tur V., Szegezdi E., et al. Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the DR5 receptor. Proceedings of the National Academy of Sciences. 2006;103(23):8634–8639. doi: 10.1073/pnas.0510187103.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Lee Y.J., Chung B.Y., Kang I.S., et al. Differential Expression of TRAIL Receptors on Skin-Infiltrating Immune Cells During the Course of Acute Urticaria. Experimental Dermatology. 2019;28(3):354–360. doi: 10.1111/exd.13878.</mixed-citation><mixed-citation xml:lang="en">Lee Y.J., Chung B.Y., Kang I.S., et al. Differential Expression of TRAIL Receptors on Skin-Infiltrating Immune Cells During the Course of Acute Urticaria. Experimental Dermatology. 2019;28(3):354–360. doi: 10.1111/exd.13878.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang L., Cheng X., Song Y., et al. Reduced expression of TRAIL-R1 and increased expression of TRAIL-R2 contribute to pathogenesis of chronic spontaneous urticaria. European Annals of Allergy and Clinical Immunology. 2018;50(1):22–28. doi: 10.23822/EurAnnACI.1764-1489.43.</mixed-citation><mixed-citation xml:lang="en">Zhang L., Cheng X., Song Y., et al. Reduced expression of TRAIL-R1 and increased expression of TRAIL-R2 contribute to pathogenesis of chronic spontaneous urticaria. European Annals of Allergy and Clinical Immunology. 2018;50(1):22–28. doi: 10.23822/EurAnnACI.1764-1489.43.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Altrichter S., Fok J.S., Jiao Q., et al. Total IgE as a Marker for Chronic Spontaneous Urticaria. Allergy, Asthma &amp; Immunology Research. 2021;13(2):206–218. doi: 10.4168/aair.2021.13.2.206.</mixed-citation><mixed-citation xml:lang="en">Altrichter S., Fok J.S., Jiao Q., et al. Total IgE as a Marker for Chronic Spontaneous Urticaria. Allergy, Asthma &amp; Immunology Research. 2021;13(2):206–218. doi: 10.4168/aair.2021.13.2.206.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Gibbs B.F., Rathling A., Zillikens D., Huber M., Haas H. Initial Fc? RI–Mediated Signal Strength Plays a Key Role in Regulating Basophil Signaling and Deactivation. Journal of Allergy and Clinical Immunology. 2006;118(5):1060–1067. doi: 10.1016/j.jaci.2006.07.012.</mixed-citation><mixed-citation xml:lang="en">Gibbs  B.F., Rathling  A., Zillikens  D., Huber  M., Haas H. Initial Fc? RI–Mediated Signal Strength Plays a  Key Role in Regulating Basophil Signaling and Deactivation. Journal of Allergy and Clinical Immunology. 2006;118(5):1060–1067. doi: 10.1016/j.jaci.2006.07.012.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Secchiero P., Melloni E., di Iasio M.G., et al. TRAIL regulates normal erythroid maturation through an ERK-dependent pathway. Blood. 2004;103(2):517–522. doi: 10.1182/blood-2003-05-1455.</mixed-citation><mixed-citation xml:lang="en">Secchiero  P., Melloni  E., di Iasio  M.G., et al. TRAIL regulates normal erythroid maturation through an ERK-dependent pathway. Blood. 2004;103(2):517–522. doi: 10.1182/blood-2003-05-1455.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Maurer M., Weller K., Bindslev-Jensen C., et al. Unmet Clinical Needs in Chronic Spontaneous Urticaria. A GA? LEN Task Force Report. Allergy. 2011;66(3):317– 330. doi: 10.1111/j.1398-9995.2010.02496.x.</mixed-citation><mixed-citation xml:lang="en">Maurer  M., Weller  K., Bindslev-Jensen  C., et al. Unmet Clinical Needs in Chronic Spontaneous Urticaria. A GA? LEN Task Force Report. Allergy. 2011;66(3):317– 330. doi: 10.1111/j.1398-9995.2010.02496.x.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Kolkhir P., Altrichter S., Asero R., et al. Autoimmune Diseases Are Linked to Type IIb Autoimmune Chronic Spontaneous Urticaria. Allergy, Asthma &amp; Immunology Research. 2021;13(4):545–559. doi: 10.4168/aair.2021.13.4.545.</mixed-citation><mixed-citation xml:lang="en">Kolkhir P., Altrichter S., Asero R., et al. Autoimmune Diseases Are Linked to Type IIb Autoimmune Chronic Spontaneous Urticaria. Allergy, Asthma &amp; Immunology Research. 2021;13(4):545–559. doi: 10.4168/aair.2021.13.4.545.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Metz M., Altrichter S., Buttgereit T., et al. The Diagnostic Workup in Chronic Spontaneous Urticaria — What to Test and Why. The Journal of Allergy and Clinical Immunology: In Practice. 2021;9(6):2274–2283. doi: 10.1016/j.jaip.2021.02.051.</mixed-citation><mixed-citation xml:lang="en">Metz  M., Altrichter  S., Buttgereit  T., et al. The Diagnostic Workup in Chronic Spontaneous Urticaria — What to Test and Why. The Journal of Allergy and Clinical Immunology: In Practice. 2021;9(6):2274–2283. doi: 10.1016/j.jaip.2021.02.051.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Vonakis B.M., Vasagar K., Gibbons S.P. Jr., et al. Basophil Fc? RI Histamine Release Parallels Expression of Src-Homology 2-Containing Inositol Phosphatases in Chronic Idiopathic Urticaria. Journal of Allergy and Clinical Immunology. 2007;119(2):441–448. doi: 10.1016/j.jaci.2006.09.035.</mixed-citation><mixed-citation xml:lang="en">Vonakis  B.M., Vasagar  K., Gibbons  S.P.  Jr., et al. Basophil Fc? RI Histamine Release Parallels Expression of Src-Homology 2-Containing Inositol Phosphatases in Chronic Idiopathic Urticaria. Journal of Allergy and Clinical Immunology. 2007;119(2):441–448. doi: 10.1016/j.jaci.2006.09.035.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Bradding P., Roberts J.A., Britten K.M., et al. Interleukin 4, –5, and –6 and Tumor Necrosis Factor-alpha in Normal and Asthmatic Airways: Evidence for the Human Mast Cell as a Source of These Cytokines. American Journal of Respiratory Cell and Molecular Biology. 1994;10(5):471–480. doi: 10.1165/ajrcmb.10.5.8179909.</mixed-citation><mixed-citation xml:lang="en">Bradding P., Roberts J.A., Britten K.M., et al. Interleukin 4, –5, and –6 and Tumor Necrosis Factor-alpha in Normal and Asthmatic Airways: Evidence for the Human Mast Cell as a Source of These Cytokines. American Journal of Respiratory Cell and Molecular Biology. 1994;10(5):471–480. doi: 10.1165/ajrcmb.10.5.8179909.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Curto-Barredo L., Pujol R.M., Roura-Vives G., GimenezArnau A.M. Chronic Urticaria Phenotypes: Clinical Differences Regarding Triggers, Activity, Prognosis and Therapeutic Response. European Journal of Dermatology. 2019;29(6):627–635. doi: 10.1684/ejd.2019.3680.</mixed-citation><mixed-citation xml:lang="en">Curto-Barredo L., Pujol R.M., Roura-Vives G., GimenezArnau  A.M.  Chronic Urticaria Phenotypes: Clinical Differences Regarding Triggers, Activity, Prognosis and Therapeutic Response. European Journal of Dermatology. 2019;29(6):627–635. doi: 10.1684/ejd.2019.3680.</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Петров В.И., Симбирцев А.С. Возрастные особенности иммунного ответа у детей. Иммунопатология, аллергология, инфектология. 2018;4:17–25.</mixed-citation><mixed-citation xml:lang="en">Petrov V.I., Simbirtsev A.S. Age-related features of the immune response in children. Immunopathology, Allergology, Infectology. 2018;4:17–25. (In Russ.).</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
