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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">mrj</journal-id><journal-title-group><journal-title xml:lang="ru">Современная ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Modern Rheumatology Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1996-7012</issn><issn pub-type="epub">2310-158X</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1996-7012-2021-5-12-17</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-1191</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>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL INVESTIGATIONS</subject></subj-group></article-categories><title-group><article-title>Экспрессия интерферон-стимулированных генов у пациентов с ревматоидным артритом на фоне анти-В-клеточной терапии (предварительные результаты)</article-title><trans-title-group xml:lang="en"><trans-title>Expression of interferon-stimulated genes in patients with rheumatoid arthritis on anti-B-cell therapy (preliminary results)</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3057-9175</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Авдеева</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Avdeeva</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Анастасия Сергеевна Авдеева</p><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><email xlink:type="simple">9056249400@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/0000-0001-7312-2349</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Четина</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Chetina</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-5946-5695</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Маркова</surname><given-names>Г. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Markova</surname><given-names>G. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1598-8360</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Насонов</surname><given-names>Е. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Nasonov</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p><p>119991, Москва, ул. Трубецкая, 8, стр. 2</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p><p>28, Trubetskaya Street, Build. 2, Moscow 119991</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»<country>Россия</country></aff><aff xml:lang="en">V.A. Nasonova Research Institute of Rheumatology<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»; Кафедра ревматологии ИПО ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)<country>Россия</country></aff><aff xml:lang="en">V.A. Nasonova Research Institute of Rheumatology; Department of Rheumatology, I.M. Sechenov First Moscow State Medical University (Sechenov University), Ministry of Health of Russia<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>19</day><month>10</month><year>2021</year></pub-date><volume>15</volume><issue>5</issue><fpage>12</fpage><lpage>17</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Авдеева А.С., Четина Е.В., Маркова Г.А., Насонов Е.Л., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Авдеева А.С., Четина Е.В., Маркова Г.А., Насонов Е.Л.</copyright-holder><copyright-holder xml:lang="en">Avdeeva A.S., Chetina E.V., Markova G.A., Nasonov E.L.</copyright-holder><license 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://mrj.ima-press.net/mrj/article/view/1191">https://mrj.ima-press.net/mrj/article/view/1191</self-uri><abstract><p>Цель исследования – оценить экспрессию интерферон-стимулированных генов (ИСГ) – интерфероновый (ИФН) «автограф» – у пациентов с ревматоидным артритом (РА) и ее динамику на фоне анти-В-клеточной терапии.Пациенты и методы. Обследовано 20 больных РА, получивших две инфузии биоаналога ритуксимаба (РТМ) Ацеллбия® в суммарной дозе 1200 мг. Для оценки ИФН-«автографа» были отобраны пять генов: IFI44L, MX1, IFIT1, RSAD2, EPSTI1. Экспрессию IFI44L и IFIT1 определить не удалось по техническим причинам и в дальнейшем анализе учитывали три гена – MX1, EPSTI1, RSAD2. ИФН-«автограф» был рассчитан как среднее значение экспрессии трех выбранных генов (ИФН-score).Результаты и обсуждение. Исходный уровень экспрессии MX1 – 11,48 (5,45–19,38), EPSTI1 – 12,83 (5,62–19,64), RSAD2 – 5,16 (2,73–10,4) и ИФН- score – 10,3 (5,18–17,12) у пациентов с РА были статистически значимо выше, чем у здоровых доноров: 1,26 (0,73–1,6); 1,06 (0,81–1,48); 0,93 (0,72–1,19) и 1,09 (0,92–1,42) соответственно (р&lt;0,05). Показатель ИФН-score был высоким у 15 (75%) больных, низким – у 5 (15%). Применение РТМ сопровождалось статистически значимым снижением активности заболевания и уровня острофазовых показателей (СОЭ, СРБ) через 12 и 24 нед терапии (p&lt;0,05). В группе в целом, а также у пациентов с умеренным эффектом терапии или его отсутствием к 24-й неделе лечения отмечались повышение экспрессии RSAD2 (p&lt;0,05) и тенденция к повышению уровня ИФН-score (р=0,06).Заключение. У пациентов с РА выявлена повышенная экспрессия ИСГ по сравнению со здоровыми донорами. При удовлетворительном эффекте РТМ или его отсутствии наблюдается повышение экспрессии RSAD2 и ИФН-score. Полученные результаты могут иметь значение для прогнозирования течения заболевания и персонификации терапии.</p></abstract><trans-abstract xml:lang="en"><p>Objective: to evaluate the expression of interferon-stimulated genes (ISG) – interferon (IFN) signature – in patients with rheumatoid arthritis (RA) and its dynamics during anti-B-cell therapy.Patients and methods.We examined 20 patients with RA who received two infusions of the biosimilar rituximab (RTM) Acellbia® in a total dose of 1200 mg. Five genes were selected to evaluate IFN signature: IFI44L, MX1, IFIT1, RSAD2, EPSTI1. The expression of IFI44L and IFIT1 could not be determined for technical reasons, and further analysis included three genes – MX1, EPSTI1, RSAD2. IFN signature was calculated as the average value of the expression of three selected genes (IFN-score).Results and discussion. The initial expression level of MX1 was 11.48 (5.45–19.38), EPSTI1 – 12.83 (5.62–19.64), RSAD2 – 5.16 (2.73–10.4) and IFN-score –10.3 (5.18–17.12), in patients with RA it was statistically significantly higher than in healthy donors: 1.26 (0.73–1.6); 1.06 (0.81–1.48); 0.93 (0.72–1.19) and 1.09 (0.92–1.42), respectively (p&lt;0.05). The IFN-score was high in 15 (75%) patients, low in 5 (15%). The use of RTM was accompanied by a statistically significant decrease in disease activity and the level of acute phase parameters (ESR, CRP) after 12 and 24 weeks of therapy (p&lt;0.05). In the group as a whole, as well as in patients with a moderate effect of therapy or its absence, by the 24th week of treatment, an increase in the expression of RSAD2 (p&lt;0.05) and a tendency to an increase in the IFN-score level (p=0.06) were observed.Conclusion. In patients with RA, an increased expression of ISH was found compared to healthy donors. An increase in the expression of RSAD2 and IFN-score is observed both in patients with a satisfactory effect of RTM and with no effect. The obtained results can be important for predicting the course of the disease and personalizing therapy.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ревматоидный артрит</kwd><kwd>интерферон-стимулированные гены</kwd><kwd>интерфероновый «автограф»</kwd><kwd>активность заболевания</kwd><kwd>эффективность терапии</kwd></kwd-group><kwd-group xml:lang="en"><kwd>rheumatoid arthritis</kwd><kwd>interferon-stimulated genes</kwd><kwd>interferon signature</kwd><kwd>disease activity</kwd><kwd>the effectiveness of therapy</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Насонов ЕЛ, Каратеев ДЕ, Балабанова РМ. Ревматоидный артрит. В кн.: Насонов ЕЛ, Насонова ВА, редакторы. Ревматология. Национальное руководство. Москва: Гэотар-Медиа; 2008. С. 290-331.</mixed-citation><mixed-citation xml:lang="en">Nasonov EL, Karateev DE, Balabanova RM. Rheumatoid arthritis. In: Nasonov EL, Nasonova VA, editors. Revmatologiya. Natsional'noe rukovodstvo [Rheumatology. National guidelines]. Moscow: Geotar-Media; 2008. P. 290-331.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Насонов ЕЛ, Авдеева АС. Иммуновоспалительные ревматические заболевания, связанные с интерфероном типа I: новые данные. Научно-практическая ревматология. 2019;57(4):452-61.</mixed-citation><mixed-citation xml:lang="en">Nasonov EL, Avdeeva AS. Immunoinflammatory Rheumatic Diseases Associated With Type I Interferon: New Evidence. Nauchno-prakticheskaya revmatologiya. 2019;57(4):452-61. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">De Weerd NA, Nguyen T. The interferons and their receptors—distribution and regulation. Immunol Cell Biol. 2012 May;90(5): 483-91. doi: 10.1038/icb.2012.9. Epub 2012 Mar 13.</mixed-citation><mixed-citation xml:lang="en">De Weerd NA, Nguyen T. The interferons and their receptors—distribution and regulation. Immunol Cell Biol. 2012 May;90(5): 483-91. doi: 10.1038/icb.2012.9. Epub 2012 Mar 13.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Hall JC, Rosen A. Type I interferons: crucial participants in disease amplification in autoimmunity. Nat Rev Rheumatol. 2010 Jan; 6(1):40-9. doi: 10.1038/nrrheum.2009.237.</mixed-citation><mixed-citation xml:lang="en">Hall JC, Rosen A. Type I interferons: crucial participants in disease amplification in autoimmunity. Nat Rev Rheumatol. 2010 Jan; 6(1):40-9. doi: 10.1038/nrrheum.2009.237.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Kotenko SV, Gallagher G, Baurin VV, et al. IFN- λs mediate antiviral protection through a distinct class II cytokine receptor complex. Nat Immunol. 2003 Jan;4(1):69-77. doi: 10.1038/ni875. Epub 2002 Dec 16.</mixed-citation><mixed-citation xml:lang="en">Kotenko SV, Gallagher G, Baurin VV, et al. IFN- λs mediate antiviral protection through a distinct class II cytokine receptor complex. Nat Immunol. 2003 Jan;4(1):69-77. doi: 10.1038/ni875. Epub 2002 Dec 16.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Ank N, West H, Bartholdy C, et al. Lambda interferon (IFN-λ), a type III IFN, is induced by viruses and IFNs and displays potent antiviral activity against select virus infections in vivo. J Virol. 2006 May;80(9): 4501-9. doi: 10.1128/JVI.80.9.4501-4509.2006.</mixed-citation><mixed-citation xml:lang="en">Ank N, West H, Bartholdy C, et al. Lambda interferon (IFN-λ), a type III IFN, is induced by viruses and IFNs and displays potent antiviral activity against select virus infections in vivo. J Virol. 2006 May;80(9): 4501-9. doi: 10.1128/JVI.80.9.4501-4509.2006.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Honda K, Takaoka A, Taniguchi T. Type I interferon gene induction by the interferon regulatory factor family of transcription factors. Immunity. 2006 Sep;25(3):349-60. doi: 10.1016/j.immuni.2006.08.009.</mixed-citation><mixed-citation xml:lang="en">Honda K, Takaoka A, Taniguchi T. Type I interferon gene induction by the interferon regulatory factor family of transcription factors. Immunity. 2006 Sep;25(3):349-60. doi: 10.1016/j.immuni.2006.08.009.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Jego G, Palucka AK, Blanck JP, et al. Plasmacytoid dendritic cells induce plasma cell differentiation through type I interferon and interleukin 6. Immunity. 2003 Aug; 19(2):225-34. doi: 10.1016/s1074-7613 (03)00208-5.</mixed-citation><mixed-citation xml:lang="en">Jego G, Palucka AK, Blanck JP, et al. Plasmacytoid dendritic cells induce plasma cell differentiation through type I interferon and interleukin 6. Immunity. 2003 Aug; 19(2):225-34. doi: 10.1016/s1074-7613 (03)00208-5.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Longhi MP, Trumpfheller C, Idoyaga J, et al. Dendritic cells require a systemic type I interferon response to mature and induce CD4+ Th1 immunity with poly IC as adjuvant. J Exp Med. 2009 Jul 6;206(7):1589-602. doi: 10.1084/jem.20090247. Epub 2009 Jun 29.</mixed-citation><mixed-citation xml:lang="en">Longhi MP, Trumpfheller C, Idoyaga J, et al. Dendritic cells require a systemic type I interferon response to mature and induce CD4+ Th1 immunity with poly IC as adjuvant. J Exp Med. 2009 Jul 6;206(7):1589-602. doi: 10.1084/jem.20090247. Epub 2009 Jun 29.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Green DS, Young HA, Valencia JC. Current prospects of type II interferon γ signaling and autoimmunity. J Biol Chem. 2017 Aug 25;292(34):13925-33. doi: 10.1074/jbc.R116.774745. Epub 2017 Jun 26.</mixed-citation><mixed-citation xml:lang="en">Green DS, Young HA, Valencia JC. Current prospects of type II interferon γ signaling and autoimmunity. J Biol Chem. 2017 Aug 25;292(34):13925-33. doi: 10.1074/jbc.R116.774745. Epub 2017 Jun 26.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Le Bon A, Thompson C, Kamphuis E, et al. Cutting edge: enhancement of antibody responses through direct stimulation of B and T cells by type I IFN. J Immunol. 2006 Feb 15;176(4):2074-8. doi: 10.4049/jimmunol.176.4.2074.</mixed-citation><mixed-citation xml:lang="en">Le Bon A, Thompson C, Kamphuis E, et al. Cutting edge: enhancement of antibody responses through direct stimulation of B and T cells by type I IFN. J Immunol. 2006 Feb 15;176(4):2074-8. doi: 10.4049/jimmunol.176.4.2074.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Psarras A, Emery P, Vital EM. Type I interferon-mediated autoimmune diseases: pathogenesis, diagnosis and targeted therapy. Rheumatology (Oxford). 2017 Oct 1;56(10): 1662-75. doi: 10.1093/rheumatology/kew431.</mixed-citation><mixed-citation xml:lang="en">Psarras A, Emery P, Vital EM. Type I interferon-mediated autoimmune diseases: pathogenesis, diagnosis and targeted therapy. Rheumatology (Oxford). 2017 Oct 1;56(10): 1662-75. doi: 10.1093/rheumatology/kew431.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Crow YJ. Type I interferonopathies: a novel set of inborn errors of immunity: type I interferonopathies. Ann N Y Acad Sci. 2011 Nov;1238:91-8. doi: 10.1111/j.1749-6632.2011.06220.x.</mixed-citation><mixed-citation xml:lang="en">Crow YJ. Type I interferonopathies: a novel set of inborn errors of immunity: type I interferonopathies. Ann N Y Acad Sci. 2011 Nov;1238:91-8. doi: 10.1111/j.1749-6632.2011.06220.x.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Ioannou Y, Isenberg DA. Current evidence for the induction of autoimmune rheumatic manifestations by cytokine therapy. Arthritis Rheum. 2000 Jul;43(7):1431-42. doi: 10.1002/1529-0131(200007)43:7&lt;1431:: AID-ANR3&gt;3.0.CO;2-E.</mixed-citation><mixed-citation xml:lang="en">Ioannou Y, Isenberg DA. Current evidence for the induction of autoimmune rheumatic manifestations by cytokine therapy. Arthritis Rheum. 2000 Jul;43(7):1431-42. doi: 10.1002/1529-0131(200007)43:7&lt;1431:: AID-ANR3&gt;3.0.CO;2-E.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Thurlings RM, Boumans M, Tekstra J, et al. Relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis patients. Arthritis Rheum. 2010 Dec;62(12):3607-14. doi: 10.1002/art.27702.</mixed-citation><mixed-citation xml:lang="en">Thurlings RM, Boumans M, Tekstra J, et al. Relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis patients. Arthritis Rheum. 2010 Dec;62(12):3607-14. doi: 10.1002/art.27702.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Raterman HG, Vosslamber S, De RS, et al. The interferon type I signature towards prediction of non-response to rituximab in rheumatoid arthritis patients. Arthritis Res Ther. 2012 Apr 27;14(2):R95. doi: 10.1186/ar3819.</mixed-citation><mixed-citation xml:lang="en">Raterman HG, Vosslamber S, De RS, et al. The interferon type I signature towards prediction of non-response to rituximab in rheumatoid arthritis patients. Arthritis Res Ther. 2012 Apr 27;14(2):R95. doi: 10.1186/ar3819.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Tchetina EV, Poole AR, EM Zaitseva, et al. Differences in mTOR (mammalian target of rapamycin) gene expression in the peripheral blood and articular cartilages of osteoarthritic patients and disease activity. Arthritis. 2013;2013:461486. doi: 10.1155/2013/461486. Epub 2013 Jun 25.</mixed-citation><mixed-citation xml:lang="en">Tchetina EV, Poole AR, EM Zaitseva, et al. Differences in mTOR (mammalian target of rapamycin) gene expression in the peripheral blood and articular cartilages of osteoarthritic patients and disease activity. Arthritis. 2013;2013:461486. doi: 10.1155/2013/461486. Epub 2013 Jun 25.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Lubbers J, Brink M, van de Stadt LA, et al. The type I IFN signature as a biomarker of preclinical rheumatoid arthritis. Ann Rheum Dis. 2013 May;72(5):776-80. doi: 10.1136/annrheumdis-2012-202753. Epub 2013 Feb 23.</mixed-citation><mixed-citation xml:lang="en">Lubbers J, Brink M, van de Stadt LA, et al. The type I IFN signature as a biomarker of preclinical rheumatoid arthritis. Ann Rheum Dis. 2013 May;72(5):776-80. doi: 10.1136/annrheumdis-2012-202753. Epub 2013 Feb 23.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Van der Pouw Kraan TC, Wijbrandts CA, van Baarsen LG, et al. Rheumatoid arthritis subtypes identified by genomic profiling of peripheral blood cells: assignment of a type I interferon signature in a subpopulation of patients. Ann Rheum Dis. 2007 Aug;66(8): 1008-14. doi: 10.1136/ard.2006.063412. Epub 2007 Jan 12.</mixed-citation><mixed-citation xml:lang="en">Van der Pouw Kraan TC, Wijbrandts CA, van Baarsen LG, et al. Rheumatoid arthritis subtypes identified by genomic profiling of peripheral blood cells: assignment of a type I interferon signature in a subpopulation of patients. Ann Rheum Dis. 2007 Aug;66(8): 1008-14. doi: 10.1136/ard.2006.063412. Epub 2007 Jan 12.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Higgs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis. 2011 Nov;70(11): 2029-36. doi: 10.1136/ard.2011.150326. Epub 2011 Jul 28.</mixed-citation><mixed-citation xml:lang="en">Higgs BW, Liu Z, White B, et al. Patients with systemic lupus erythematosus, myositis, rheumatoid arthritis and scleroderma share activation of a common type I interferon pathway. Ann Rheum Dis. 2011 Nov;70(11): 2029-36. doi: 10.1136/ard.2011.150326. Epub 2011 Jul 28.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-β/α ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort. Arthritis Rheum. 2010 Feb;62(2):392-401. doi: 10.1002/art.27226.</mixed-citation><mixed-citation xml:lang="en">Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to tumor necrosis factor antagonists with plasma type I interferon activity and interferon-β/α ratios in rheumatoid arthritis patients: a post hoc analysis of a predominantly Hispanic cohort. Arthritis Rheum. 2010 Feb;62(2):392-401. doi: 10.1002/art.27226.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Wampler Muskardin T, Vashisht P, Dorschner JM, et al. Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis. Ann Rheum Dis. 2016 Oct;75(10):1757-62. doi: 10.1136/annrheumdis-2015-208001. Epub 2015 Nov 6.</mixed-citation><mixed-citation xml:lang="en">Wampler Muskardin T, Vashisht P, Dorschner JM, et al. Increased pretreatment serum IFN-β/α ratio predicts non-response to tumour necrosis factor α inhibition in rheumatoid arthritis. Ann Rheum Dis. 2016 Oct;75(10):1757-62. doi: 10.1136/annrheumdis-2015-208001. Epub 2015 Nov 6.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">De Jong TD, Vosslamber S, Mantel E, et al. Physiological evidence for diversification of IFNα- and IFNβ-mediated response programs in different autoimmune diseases. Arthritis Res Ther. 2016 Feb 17;18:49. doi: 10.1186/s13075-016-0946-9.</mixed-citation><mixed-citation xml:lang="en">De Jong TD, Vosslamber S, Mantel E, et al. Physiological evidence for diversification of IFNα- and IFNβ-mediated response programs in different autoimmune diseases. Arthritis Res Ther. 2016 Feb 17;18:49. doi: 10.1186/s13075-016-0946-9.</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>
