<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Vestnik dermatologii i venerologii</journal-id><journal-title-group><journal-title xml:lang="en">Vestnik dermatologii i venerologii</journal-title><trans-title-group xml:lang="ru"><trans-title>Вестник дерматологии и венерологии</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0042-4609</issn><issn publication-format="electronic">2313-6294</issn><publisher><publisher-name xml:lang="en">Rossijskoe Obschestvo Dermatovenerologov i Kosmetologov</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1362</article-id><article-id pub-id-type="doi">10.25208/vdv1362</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>REVIEWS</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ОБЗОР ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">HLA-B27 and its role in the pathogenesis of psoriatic arthritis</article-title><trans-title-group xml:lang="ru"><trans-title>Значение HLA-B27 в патогенезе псориатического артрита</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3778-4745</contrib-id><contrib-id contrib-id-type="spin">3308-3330</contrib-id><name-alternatives><name xml:lang="en"><surname>Artamonova</surname><given-names>Olga G.</given-names></name><name xml:lang="ru"><surname>Артамонова</surname><given-names>Ольга Григорьевна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>Junior Research Associate</p></bio><bio xml:lang="ru"><p>младший научный сотрудник</p></bio><email>artamonova_olga@list.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3805-8489</contrib-id><contrib-id contrib-id-type="spin">3604-6491</contrib-id><name-alternatives><name xml:lang="en"><surname>Karamova</surname><given-names>Arfenya E.</given-names></name><name xml:lang="ru"><surname>Карамова</surname><given-names>Арфеня Эдуардовна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Cand. Sci. (Med.), Assistant Professor</p></bio><bio xml:lang="ru"><p>к.м.н., доцент</p></bio><email>karamova@cnikvi.ru</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9688-2727</contrib-id><contrib-id contrib-id-type="spin">3385-4723</contrib-id><name-alternatives><name xml:lang="en"><surname>Chikin</surname><given-names>Vadim V.</given-names></name><name xml:lang="ru"><surname>Чикин</surname><given-names>Вадим Викторович</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Assistant Professor</p></bio><bio xml:lang="ru"><p>д.м.н., доцент</p></bio><email>chikin@cnikvi.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7625-0503</contrib-id><contrib-id contrib-id-type="spin">8771-4990</contrib-id><name-alternatives><name xml:lang="en"><surname>Kubanov</surname><given-names>Alexey A.</given-names></name><name xml:lang="ru"><surname>Кубанов</surname><given-names>Алексей Алексеевич</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Dr. Sci. (Med.), Professor, Academician of the Russian Academy of Sciences</p></bio><bio xml:lang="ru"><p>д.м.н., профессор, академик РАН</p></bio><email>alex@cnikvi.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">State Research Center of Dermatovenereology and Cosmetology</institution></aff><aff><institution xml:lang="ru">Государственный научный центр дерматовенерологии и косметологии</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Federal State Research Center of Dermatovenereology and Cosmetology, Moscow</institution></aff><aff><institution xml:lang="ru">Государственный научный центр дерматовенерологии и косметологии</institution></aff></aff-alternatives><pub-date date-type="preprint" iso-8601-date="2022-10-25" publication-format="electronic"><day>25</day><month>10</month><year>2022</year></pub-date><pub-date date-type="pub" iso-8601-date="2022-11-23" publication-format="electronic"><day>23</day><month>11</month><year>2022</year></pub-date><volume>98</volume><issue>5</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>34</fpage><lpage>44</lpage><history><date date-type="received" iso-8601-date="2022-08-31"><day>31</day><month>08</month><year>2022</year></date><date date-type="accepted" iso-8601-date="2022-09-06"><day>06</day><month>09</month><year>2022</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2022, Artamonova O.G., Karamova A.E., Chikin V.V., Kubanov A.A.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2022, Артамонова О.Г., Карамова А.Э., Чикин В.В., Кубанов А.А.</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="en">Artamonova O.G., Karamova A.E., Chikin V.V., Kubanov A.A.</copyright-holder><copyright-holder xml:lang="ru">Артамонова О.Г., Карамова А.Э., Чикин В.В., Кубанов А.А.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://vestnikdv.ru/jour/article/view/1362">https://vestnikdv.ru/jour/article/view/1362</self-uri><abstract xml:lang="en"><p>The literature review presents the characteristics of the human leukocyte antigen (HLA)-B27 as a factor contributing to the development of psoriatic arthritis. HLA-B27 is a class I surface antigen encoded by the major histocompatibility complex (MHC) B locus located on chromosome 6. The main function is to present antigenic peptides to the CD8+ T-cells. HLA-B27 is the most important genetic biomarker for psoriatic arthritis, as it provides phenotypic differentiation in the patient population. The prevalence of <italic>HLA-B*27</italic> in various population groups are presented. The structural features of the HLA-B27 molecule are described. The characteristics of methods for detecting <italic>HLA-B*27</italic> status and determining its subtypes are given. The main mechanisms of the <italic>HLA-B*27 </italic>polymorphism influence on the development of psoriatic arthritis are considered, and hypotheses are analyzed that explain the pathogenic effect of <italic>HLA-B*27</italic>: the arthritogenic peptide hypothesis, the misfolding hypothesis, the HLA-B27 heavy chain homodimer formation hypothesis. The features of the clinical manifestations and course of <italic>HLA-B*27</italic>-positive psoriatic arthritis are presented, allowing the use of HLA-B27 to predict the development of psoriatic joint damage.</p></abstract><trans-abstract xml:lang="ru"><p>В обзоре литературы представлена характеристика человеческого лейкоцитарного антигена (HLA)-B27 как фактора, способствующего развитию псориатического артрита. HLA-B27 представляет собой поверхностный антиген класса I, кодируемый геном <italic>HLA-B*27</italic>, расположенным на локусе B главного комплекса гистосовместимости (MHC) на 6-й хромосоме. Основная функция заключается в представлении эндогенных (внутриклеточных) пептидов Т-клеточному рецептору CD8+ цитотоксических Т-лимфоцитов. HLA-B27 — важнейший генетический биомаркер псориатического артрита, обеспечивающий фенотипическую дифференциацию в популяции больных. Представлены данные о носительстве гена <italic>HLA-B*27</italic> в различных группах населения. Описаны особенности строения молекулы HLA-B27. Дана характеристика методов выявления носительства <italic>HLA-B*27</italic> и определения его вариантов. Рассмотрены основные механизмы влияния полиморфизма <italic>HLA-B*27</italic> на развитие псориатического артрита и проведен анализ гипотез, объясняющих патогенный эффект носительства <italic>HLA-B*27</italic> формированием артритогенных пептидов, неправильным свертыванием молекулы HLA-B27, образованием ее гомодимеров. Представлены данные об особенностях развития, клинических проявлений и течения псориатического артрита у носителей <italic>HLA-B*27</italic>, позволяющие использовать HLA-B27 для прогнозирования развития псориатического поражения суставов.</p></trans-abstract><kwd-group xml:lang="en"><kwd>psoriatic arthritis</kwd><kwd>HLA genes</kwd><kwd>HLA-B*27</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>псориатический артрит</kwd><kwd>гены системы HLA</kwd><kwd>HLA-B*27</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Коротаева Т.В., Корсакова Ю.Л. Псориатический артрит: классификация, клиническая картина, диагностика, лечение. Научно-практическая ревматология. 2018;56(1):60–69 [Korotaeva TV, Korsakova YuL. Psoriatic arthritis: classification, clinical presentation, diagnosis, treatment. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2018;56(1):60–69. (In Russ.)]. doi: 10.14412/1995-4484-2018-60-69</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Veale DJ, Fearon U. The pathogenesis of psoriatic arthritis. Lancet. 2018;391(10136):2273–2284. doi: 10.1016/S0140-6736(18)30830-4</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Moll JM, Wright V. Psoriatic arthritis. Semin Arthritis Rheum. 1973;3(1):55–78. doi: 10.1016/0049-0172(73)90035-8</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H; CASPAR Study Group. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. 2006;54(8):2665–2673. doi: 10.1002/art.21972</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Баткаева Н.В., Коротаева Т.В., Баткаев Э.А. Разнообразие коморбидной патологии у больных псориазом тяжелого течения. Альманах клинической медицины. 2018;46(1):76–81. [Batkaeva NV, Korotaeva TV, Batkaev EA. Multiplicity of comorbidities in patients with severe psoriasis. Almanac of Clinical Medicine. 2018;46(1):76–81. (In Russ.)]. doi: 10.18786/2072-0505-2018-46-1-76-81</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Ogdie A, Schwartzman S, Husni ME. Recognizing and managing comorbidities in psoriatic arthritis. Curr Opin Rheumatol. 2015;27(2):118–126. doi: 10.1097/BOR.0000000000000152</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Michelsen B, Fiane R, Diamantopoulos AP, Soldal DM, Hansen IJ, Sokka T, Kavanaugh A, Haugeberg G. A comparison of disease burden in rheumatoid arthritis, psoriatic arthritis and axial spondyloarthritis. PLoS One. 2015;10(4):e0123582. doi: 10.1371/journal.pone.0123582</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Tillett W, Shaddick G, Askari A, Cooper A, Creamer P, Clunie G, et al. Factors influencing work disability in psoriatic arthritis: first results from a large UK multicentre study. Rheumatology (Oxford). 2015;54(1):157–162. doi: 10.1093/rheumatology/keu264</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Skov L, Thomsen SF, Kristensen LE, Dodge R, Hedegaard MS, Kjellberg J. Cause-specific mortality in patients with psoriasis and psoriatic arthritis. Br J Dermatol. 2019;180(1):100–107. doi: 10.1111/bjd.16919</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Кубанов А.А., Карамова А.Э., Чикин В.В., Вербенко Д.А., Знаменская Л.Ф., Артамонова О.Г. Генетические маркеры развития псориатического поражения суставов у больных псориазом. Часть I: Полиморфизмы генома, не относящиеся к системе HLA. Вестник дерматологии и венерологии. 2021;97(4):33–47. [Kubanov AA, Karamova AE, Chikin VV, Verbenko DA, Znamenskaya LF, Artamonova OG. Genetic markers for psoriatic arthritis in patients with psoriasis. Part I: non-HLA genes. Vestnik dermatologii i venerologii. 2021;97(4):33–47. (In Russ.)]. doi: 10.25208/vdv1269</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Кубанов А.А., Чикин В.В., Карамова А.Э., Знаменская Л.Ф., Артамонова О.Г., Вербенко Д.А. Генетические маркеры развития поражения суставов у больных псориазом. Часть II: Гены системы HLA. Вестник дерматологии и венерологии. 2021;97(5):6–17. [Kubanov AA, Chikin VV, Karamova AE, Znamenskaya LF, Artamonova OG, Verbenko DA. Genetic markers for psoriatic arthritis among patients with psoriasis. Part II: HLA genes. Vestnik dermatologii i venerologii. 2021;97(5):6–17. (In Russ.)]. doi: 10.25208/vdv1269</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Shankarkumar U. The Human Leukocyte Antigen (HLA) System, International Journal of Human Genetics, 2004;4:2,91–103. doi: 10.1080/09723757.2004.11885875</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Trowsdale J, Knight JC. Major histocompatibility complex genomics and human disease. Annu Rev Genomics Hum Genet. 2013;14:301–323. doi: 10.1146/annurev-genom-091212-153455</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Robinson J, Barker DJ, Georgiou X, Cooper MA, Flicek P, Marsh SGE. IPD-IMGT/HLA Database. Nucleic Acids Res. 2020;48(D1):D948-D955. doi: 10.1093/nar/gkz950</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Wieczorek M, Abualrous ET, Sticht J, Álvaro-Benito M, Stolzenberg S, Noé F, Freund C. Major histocompatibility complex (MHC) class I and MHC class II proteins: Conformational plasticity in antigen presentation. Front Immunol. 2017;8:292. doi: 10.3389/fimmu.2017.00292</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Thorsby E. HL-A antigens and genes. I. A study of unrelated Norwegians. Vox Sang. 1969;17(2):81–92. doi: 10.1111/j.1423-0410.1969.tb00377.x</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Brewerton DA, Hart FD, Nicholls A, Caffrey M, James DC, Sturrock RD. Ankylosing spondylitis and HL-A 27. Lancet. 1973;1(7809):904–907. doi: 10.1016/s0140-6736(73)91360-3</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Schlosstein L, Terasaki PI, Bluestone R, Pearson CM. High association of an HL-A antigen, W27, with ankylosing spondylitis. N Engl J Med. 1973;288(14):704–706.</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Madden DR, Gorga JC, Strominger JL, Wiley DC. The three-dimensional structure of HLA-B27 at 2.1 A resolution suggests a general mechanism for tight peptide binding to MHC. Cell. 1992;70(6):1035–1048. doi: 10.1016/0092-8674(92)90252-8</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Jardetzky TS, Lane WS, Robinson RA, Madden DR, Wiley DC. Identification of self peptides bound to purified HLA-B27. Nature. 1991;353(6342):326-329. doi: 10.1038/353326a0</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Peh CA, Burrows SR, Barnden M, Khanna R, Cresswell P, Moss DJ, McCluskey J. HLA-B27-restricted antigen presentation in the absence of tapasin reveals polymorphism in mechanisms of HLA class I peptide loading. Immunity. 1998;8(5):531–542. doi: 10.1016/s1074-7613(00)80558-0</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Khan MA. HLA-B27 and its pathogenic role. J Clin Rheumatol. 2008;14(1):50–52. doi: 10.1097/RHU.0b013e3181637a38</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Фефелова В.В., Хамнагадаев И.И., Поликарпов Л.С. Ген HLA-B27 и спондилоартропатии у арктических монголоидов. Сибирский научный медицинский журнал. 2010;30(6):136–139. [Fefelova VV, Khamnagadaev II, Polikarpov LS. HLA-B27 antigen and spondylarthropathies in arctic mongoloids. The Siberian Scientific Medical Journal. 2010;30(6);136–139. (In Russ.)]</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Woodrow JC. Genetic aspects of the spondyloarthropathies. Clin Rheum Dis. 1985;11(1):1–24.</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Беневоленская Л.И., Бойер Д., Эрдес Ш. Сравнительное изучение спондилоартропатий среди коренных жителей Чукотки и Аляски. Терапевтический архив. 1998;(1):41–46. [Benevolenskaya LI, Boier D, Erdes Sh. Comparative investigation on epidemiology of spondyloarthropathies among Chukotka and Alaska indigenous people. Ter. arkhiv. 1998;(1):41–46. (In Russ.)]</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Mehra NK, Kaur G. The HLA complex in biology and medicine. New Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd. — 2010.</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Khan M.A. Ankylosing spondylitis. — Oxford University Press, 2009.</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>D'Amato M, Fiorillo MT, Carcassi C, Mathieu A, Zuccarelli A, Bitti PP, et al. Relevance of residue 116 of HLA-B27 in determining susceptibility to ankylosing spondylitis. Eur J Immunol. 1995;25(11):3199–3201. doi: 10.1002/eji.1830251133</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Brown MA, Jepson A, Young A, Whittle HC, Greenwood BM, Wordsworth BP. Ankylosing spondylitis in West Africans — evidence for a non-HLA-B27 protective effect. Ann Rheum Dis. 1997;56(1):68–70. doi: 10.1136/ard.56.1.68</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>Brown MA, Kennedy LG, MacGregor AJ, Darke C, Duncan E, Shatford JL, et al. Susceptibility to ankylosing spondylitis in twins: the role of genes, HLA, and the environment. Arthritis Rheum. 1997;40(10):1823–1828. doi: 10.1002/art.1780401015</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Khan MA. Polymorphism of HLA-B27: 105 subtypes currently known. Curr Rheumatol Rep. 2013;15(10):362. doi: 10.1007/s11926-013-0362-y</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Григорьева Л.В., Винокурова Ф.В., Гольдерова А.С., Николаев В.М., Бурцева Т.М., Аргунова В.М., и др. Частота HLA-B27 в Республике Саха (Якутия). Экология и здоровье человека на Севере: сборник материалов IV-го конгресса с международным участием. Россия, Якутск, Северо-Восточный федеральный университет имени М.К. Аммосова, 4–7 декабря 2013 г. 2013. С. 162. [Grigorieva LV, Vinokurova FV, Golderova AS, Nikolaev VM, Bourtseva TM, Argunova VM, et al. The frequency of HLA-B27 in the Republic of Sakha (Yakutia) // Ecology and human health in the North: collection of materials of the IV Congress with international participation. Russia, Yakutsk, North-Eastern Federal University named after MK Ammosov, December 4–7, 2013. 2013. P. 162. (In Russ.)]</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Сартакова М.Л. Изучение наиболее часто встречающихся аллелей гена HLA-B27 у тувинцев и русских жителей Западной Сибири. Генетика. 2000;35(5):710–713. [Sartakova ML. The study of the most common alleles of the HLA-B27 gene in Tuvinians and Russian residents of Western Siberia. Genetics. 2000;35(5):710–713. (In Russ.)]</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>López-Larrea C, Torre Alonso JC, Rodriguez Perez A, Coto E. HLA antigens in psoriatic arthritis subtypes of a Spanish population. Ann Rheum Dis. 1990;49(5):318–319. doi: 10.1136/ard.49.5.318</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Williamson L, Dockerty JL, Dalbeth N, McNally E, Ostlere S, Wordsworth BP. Clinical assessment of sacroiliitis and HLA-B27 are poor predictors of sacroiliitis diagnosed by magnetic resonance imaging in psoriatic arthritis. Rheumatology (Oxford). 2004;43(1):85–88. doi: 10.1093/rheumatology/keg475</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Liao HT, Lin KC, Chang YT, Chen CH, Liang TH, Chen WS, et al. Human leukocyte antigen and clinical and demographic characteristics in psoriatic arthritis and psoriasis in Chinese patients. J Rheumatol. 2008;35(5):891–895.</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Бадокин В.В., Трошкина И.А., Гусева И.А. Значение генетической компоненты в клинической презентации псориатического артрита. Доктор.Ру. 2012;2(70):44–49. [Badokin VV, Troshkina IA, Guseva IA. Psoriatic arthritis: Role of genetic component in disease’s clinical manifestation. Doktor.ru. 2012;2(70):44–49. (In Russ.)]</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>Sharma N, Sharma V, Masood T, Nautiyal SC, Sailwal S, Singh RK, et al. Usage of conventional PCR technology for the detection of HLA-B27 allele: A Significant molecular marker of ankylosing spondylitis. Indian J Clin Biochem. 2013;28(2):189–192. doi: 10.1007/s12291-012-0261-4</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Terasaki PI, Mcclelland JD. Microdroplet assay of human serum cytotoxins. Nature. 1964;204:998-1000. doi: 10.1038/204998b0</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Cianga P, Zlei M, Rezus E, Cianga C. The flow cytometric labeling pattern in HLA-B27 detection may suggest cross reactivities. Revista Română de Medicină de Laborator. 2011;19(2/4):185–191</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>Kopko PM, Eisenbrey AB, Maha GC. 144-P: College of american pathologists HLA-B 27 proficiency testing data reveals increased false positive rates for flow cytometry methods. Human Immunology. 2013;74:149</mixed-citation></ref><ref id="B42"><label>42.</label><mixed-citation>Euroimmun.com. EuroImmune, Inc. [April 2015]. Available from: https://www.euroimmun.com/documents/HLA-B27/MV_5110_D_UK_B.pdf. (Accessed August 15, 2015).</mixed-citation></ref><ref id="B43"><label>43.</label><mixed-citation>Robinson J, Barker DJ, Georgiou X, Cooper MA, Flicek P, Marsh SGE. IPD-IMGT/HLA Database Nucleic Acids Research. 2020; 48 (D1): D948-D955</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Khan MA. An Update on the Genetic Polymorphism of HLA-B*27 With 213 Alleles Encompassing 160 Subtypes (and Still Counting). Curr Rheumatol Rep. 2017;19(2):9. doi: 10.1007/s11926-017-0640-1</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Goulder PJ, Watkins DI. Impact of MHC class I diversity on immune control of immunodeficiency virus replication. Nat Rev Immunol. 2008;8(8):619–630. doi: 10.1038/nri2357</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>McKiernan SM, Hagan R, Curry M, McDonald GS, Kelly A, Nolan N, et al. Distinct MHC class I and II alleles are associated with hepatitis C viral clearance, originating from a single source. Hepatology. 2004;40(1):108–114. doi: 10.1002/hep.20261</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>MacLean IL, Iqball S, Woo P, Keat AC, Hughes RA, Kingsley GH, Knight SC. HLA-B27 subtypes in the spondarthropathies. Clin Exp Immunol. 1993;91(2):214–219. doi: 10.1111/j.1365-2249.1993.tb05885.x</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>López-Larrea C, Sujirachato K, Mehra NK, Chiewsilp P, Isarangkura D, Kanga U, et al. HLA-B27 subtypes in Asian patients with ankylosing spondylitis. Evidence for new associations. Tissue Antigens. 1995;45(3):169–176. doi: 10.1111/j.1399-0039.1995.tb02436.x</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>Armas JB, Gonzalez S, Martinez-Borra J, Laranjeira F, Ribeiro E, Correia J, et al. Susceptibility to ankylosing spondylitis is independent of the Bw4 and Bw6 epitopes of HLA-B27 alleles. Tissue Antigens. 1999;53(3):237–243. doi: 10.1034/j.1399-0039.1999.530303.x</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Gonzalez-Roces S, Alvarez MV, Gonzalez S, Dieye A, Makni H, Woodfield DG, et al. HLA-B27 polymorphism and worldwide susceptibility to ankylosing spondylitis. Tissue Antigens. 1997;49(2):116–123. doi: 10.1111/j.1399-0039.1997.tb02724.x</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>McHugh K, Bowness P. The link between HLA-B27 and SpA-new ideas on an old problem. Rheumatology (Oxford). 2012;51(9):1529–1539. doi: 10.1093/rheumatology/kes061</mixed-citation></ref><ref id="B52"><label>52.</label><mixed-citation>Robinson PC, Brown MA. The genetics of ankylosing spondylitis and axial spondyloarthritis. Rheum Dis Clin North Am. 2012;38(3):539–553. doi: 10.1016/j.rdc.2012.08.018</mixed-citation></ref><ref id="B53"><label>53.</label><mixed-citation>Colbert RA, Tran TM, Layh-Schmitt G. HLA-B27 misfolding and ankylosing spondylitis. Mol Immunol. 2014;57(1):44–51. doi: 10.1016/j.molimm.2013.07.013</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Hermann E, Yu DT, Meyer zum Büschenfelde KH, Fleischer B. HLA-B27-restricted CD8 T cells derived from synovial fluids of patients with reactive arthritis and ankylosing spondylitis. Lancet. 1993;342(8872):646–650. doi: 10.1016/0140-6736(93)91760-j</mixed-citation></ref><ref id="B55"><label>55.</label><mixed-citation>May E, Dorris ML, Satumtira N, Iqbal I, Rehman MI, Lightfoot E, Taurog JD. CD8 alpha beta T cells are not essential to the pathogenesis of arthritis or colitis in HLA-B27 transgenic rats. J Immunol. 2003;170(2):1099–1105. doi: 10.4049/jimmunol.170.2.1099</mixed-citation></ref><ref id="B56"><label>56.</label><mixed-citation>Tedeschi V, Paldino G, Paladini F, Mattorre B, Tuosto L, Sorrentino R, Fiorillo MT. The Impact of the 'Mis-Peptidome' on HLA Class I-Mediated Diseases: Contribution of ERAP1 and ERAP2 and effects on the immune response. Int J Mol Sci. 2020;21(24):9608. doi: 10.3390/ijms21249608</mixed-citation></ref><ref id="B57"><label>57.</label><mixed-citation>Colbert RA, Navid F, Gill T. The role of HLA-B*27 in spondyloarthritis. Best Pract Res Clin Rheumatol. 2017;31(6):797–815. doi: 10.1016/j.berh.2018.07.012</mixed-citation></ref><ref id="B58"><label>58.</label><mixed-citation>Dangoria NS, DeLay ML, Kingsbury DJ, Mear JP, Uchanska-Ziegler B, Ziegler A, et al. HLA-B27 misfolding is associated with aberrant intermolecular disulfide bond formation (dimerization) in the endoplasmic reticulum. J Biol Chem. 2002;277(26):23459–23468. doi: 10.1074/jbc.M110336200</mixed-citation></ref><ref id="B59"><label>59.</label><mixed-citation>Khare SD, Hansen J, Luthra HS, David CS. HLA-B27 heavy chains contribute to spontaneous inflammatory disease in B27/human beta2-microglobulin (beta2m) double transgenic mice with disrupted mouse beta2m. J Clin Invest. 1996;98(12):2746–2755. doi: 10.1172/JCI119100</mixed-citation></ref><ref id="B60"><label>60.</label><mixed-citation>Tran TM, Dorris ML, Satumtira N, Richardson JA, Hammer RE, Shang J, Taurog JD. Additional human beta2-microglobulin curbs HLA-B27 misfolding and promotes arthritis and spondylitis without colitis in male HLA-B27-transgenic rats. Arthritis Rheum. 2006; 54(4):1317–1327. doi: 10.1002/art.21740</mixed-citation></ref><ref id="B61"><label>61.</label><mixed-citation>Chan AT, Kollnberger SD, Wedderburn LR, Bowness P. Expansion and enhanced survival of natural killer cells expressing the killer immunoglobulin-like receptor KIR3DL2 in spondylarthritis. Arthritis Rheum. 2005;52(11):3586–3895. doi: 10.1002/art.21395</mixed-citation></ref><ref id="B62"><label>62.</label><mixed-citation>Lanier LL. Follow the leader: NK cell receptors for classical and nonclassical MHC class I. Cell. 1998;92(6):705–707. doi: 10.1016/s0092-8674(00)81398-7</mixed-citation></ref><ref id="B63"><label>63.</label><mixed-citation>Bowness P, Ridley A, Shaw J, Chan AT, Wong-Baeza I, Fleming M, et al. Th17 cells expressing KIR3DL2+ and responsive to HLA-B27 homodimers are increased in ankylosing spondylitis. J Immunol. 2011;186(4):2672–2680. doi: 10.4049/jimmunol.1002653</mixed-citation></ref><ref id="B64"><label>64.</label><mixed-citation>Chandran V, Bull SB, Pellett FJ, Ayearst R, Rahman P, Gladman DD. Human leukocyte antigen alleles and susceptibility to psoriatic arthritis. Hum Immunol. 2013;74(10):1333–8. doi: 10.1016/j.humimm.2013.07.014</mixed-citation></ref><ref id="B65"><label>65.</label><mixed-citation>Eder L, Chandran V, Pellet F, Shanmugarajah S, Rosen CF, Bull SB, Gladman DD. Human leucocyte antigen risk alleles for psoriatic arthritis among patients with psoriasis. Ann Rheum Dis. 2012;71(1):50–55. doi: 10.1136/ard.2011.155044</mixed-citation></ref><ref id="B66"><label>66.</label><mixed-citation>Eder L, Chandran V, Pellett F, Shanmugarajah S, Rosen CF, Bull SB, Gladman DD. Differential human leucocyte allele association between psoriasis and psoriatic arthritis: a family-based association study. Ann Rheum Dis. 2012;71(8):1361–1365. doi: 10.1136/annrheumdis-2012-201308</mixed-citation></ref><ref id="B67"><label>67.</label><mixed-citation>Winchester R, Minevich G, Steshenko V, Kirby B, Kane D, Greenberg DA, FitzGerald O. HLA associations reveal genetic heterogeneity in psoriatic arthritis and in the psoriasis phenotype. Arthritis Rheum. 2012;64(4):1134–1144. doi: 10.1002/art.33415</mixed-citation></ref><ref id="B68"><label>68.</label><mixed-citation>Minh VN, Thi VB, Van TC, Ngoc TN, Ngoc AT, Van ED, et al. The relationship between HLA-B27, HLA-Cw06, HLA-DR7 and psoriatic arthritis in vietnamese patients: Disease progression and therapeutic burden. Open Access Maced J Med Sci. 2019;7(2):300–301. doi: 10.3889/oamjms.2019.064</mixed-citation></ref><ref id="B69"><label>69.</label><mixed-citation>Alenius GM, Jidell E, Nordmark L, Rantapää Dahlqvist S. Disease manifestations and HLA antigens in psoriatic arthritis in northern Sweden. Clin Rheumatol. 2002;21(5):357–362. doi: 10.1007/s100670200097</mixed-citation></ref><ref id="B70"><label>70.</label><mixed-citation>Chandran V. (2013). Genetic determinants of psoriatic arthritis (Doctoral dissertation, University of Toronto).</mixed-citation></ref><ref id="B71"><label>71.</label><mixed-citation>Chandran V, Bull SB, Pellett FJ, Ayearst R, Rahman P, Gladman DD. Human leukocyte antigen alleles and susceptibility to psoriatic arthritis. Hum Immunol. 2013;74(10):1333–1338. doi: 10.1016/j.humimm.2013.07.014</mixed-citation></ref><ref id="B72"><label>72.</label><mixed-citation>Haroon M, Winchester R, Giles JT, Heffernan E, FitzGerald O. Certain class I HLA alleles and haplotypes implicated in susceptibility play a role in determining specific features of the psoriatic arthritis phenotype. Ann Rheum Dis. 2016;75(1):155–162. doi: 10.1136/annrheumdis-2014-205461</mixed-citation></ref><ref id="B73"><label>73.</label><mixed-citation>Gladman DD, Farewell VT. The role of HLA antigens as indicators of disease progression in psoriatic arthritis. Multivariate relative risk model. Arthritis Rheum. 1995;38(6):845–850. doi: 10.1002/art.1780380619</mixed-citation></ref><ref id="B74"><label>74.</label><mixed-citation>Queiro R, Sarasqueta C, Belzunegui J, Gonzalez C, Figueroa M, Torre-Alonso JC. Psoriatic spondyloarthropathy: a comparative study between HLA-B27 positive and HLA-B27 negative disease. Semin Arthritis Rheum. 2002;31(6):413–418. doi: 10.1053/sarh.2002.33470</mixed-citation></ref><ref id="B75"><label>75.</label><mixed-citation>Queiro R, Sarasqueta C, Torre JC, Tinturé T, López-Lagunas I. Spectrum of psoriatic spondyloarthropathy in a cohort of 100 Spanish patients. Ann Rheum Dis. 2005;61(9):857–858. doi: 10.1136/ard.61.9.857</mixed-citation></ref><ref id="B76"><label>76.</label><mixed-citation>Coates LC, Baraliakos X, Blanco FJ, Blanco-Morales EA, Braun J, Chandran V, et al. The Phenotype of Axial Spondyloarthritis: Is It Dependent on HLA-B27 Status? Arthritis Care Res (Hoboken). 2021;73(6):856–860. doi: 10.1002/acr.24174</mixed-citation></ref><ref id="B77"><label>77.</label><mixed-citation>Marzo-Ortega H, McGonagle D, O'Connor P, Hensor EM, Bennett AN, Green MJ, Emery P. Baseline and 1-year magnetic resonance imaging of the sacroiliac joint and lumbar spine in very early inflammatory back pain. Relationship between symptoms, HLA-B27 and disease extent and persistence. Ann Rheum Dis. 2009;68(11):1721–1727. doi: 10.1136/ard.2008.097931</mixed-citation></ref><ref id="B78"><label>78.</label><mixed-citation>Bennett AN, McGonagle D, O'Connor P, Hensor EM, Sivera F, Coates LC, et al. Severity of baseline magnetic resonance imaging-evident sacroiliitis and HLA-B27 status in early inflammatory back pain predict radiographically evident ankylosing spondylitis at eight years. Arthritis Rheum. 2008;58(11):3413–3418. doi: 10.1002/art.24024</mixed-citation></ref><ref id="B79"><label>79.</label><mixed-citation>Castillo-Gallego C, Aydin SZ, Emery P, McGonagle DG, Marzo-Ortega H. Magnetic resonance imaging assessment of axial psoriatic arthritis: extent of disease relates to HLA-B27. Arthritis Rheum. 2013;65(9):2274–2278. doi: 10.1002/art.38050</mixed-citation></ref><ref id="B80"><label>80.</label><mixed-citation>Логинова Е.Ю., Коротаева Т.В., Смирнов А.В., Глазков А.А., Каратеев Д.Е., Насонов Е.Л. Особенности поражения осевого скелета при раннем псориатическом артрите (исследование РЕМАРКА). Научно-практическая ревматология. 2016;54 (S1):15-19. [Loginova EJu, Korotaeva TV, Smirnov AV, Glazkov AA, Karateev DE, Nasonov EL. Specific features of axial skeletal involvement in early psoriatic arthritis (The REMARCA Trial). Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2016;54(Suppl. 1):15-19. (In Russ)]. doi: 10.14412/1995-4484-2016-1S-15-19</mixed-citation></ref><ref id="B81"><label>81.</label><mixed-citation>Губарь Е.Е., Логинова Е.Ю., Коротаева Т.В., Глухова С.И., Насонов Е.Л. Сравнительная характеристика раннего псориатического артрита с поражением и без поражения осевого скелета (субанализ общероссийского регистра пациентов с псориатическим артритом). Научно-практическая ревматология. 2019;57(6):636–641. [Gubar EE, Loginova EYu, Korotaeva TV, Glukhova SI, Nasonov EL. Comparative characteristics of early psoriatic arthritis with and without axial skeleton injury (a subanalysis of the all-Russian registry of patients with psoriatic arthritis). Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2019;57(6):636–641. (In Russ.)]. doi: 10.14412/1995-4484-2019-636-641</mixed-citation></ref><ref id="B82"><label>82.</label><mixed-citation>Eder L, Widdifield J, Rosen CF, Cook R, Lee KA, Alhusayen R, et al. Trends in the Prevalence and Incidence of Psoriasis and Psoriatic Arthritis in Ontario, Canada: A Population-Based Study. Arthritis Care Res (Hoboken). 2019;71(8):1084–1091. doi: 10.1002/acr.23743</mixed-citation></ref><ref id="B83"><label>83.</label><mixed-citation>Wei JC, Shi LH, Huang JY, Wu XF, Wu R, Chiou JY. Epidemiology and medication pattern change of psoriatic diseases in Taiwan from 2000 to 2013: A nationwide, population-based cohort study. J Rheumatol. 2018;45(3):385–392. doi: 10.3899/jrheum.170516</mixed-citation></ref><ref id="B84"><label>84.</label><mixed-citation>Eder L, Cohen AD, Feldhamer I, Greenberg-Dotan S, Batat E, Zisman D. The epidemiology of psoriatic arthritis in Israel — a population-based study. Arthritis Res Ther. 2018;20(1):3. doi: 10.1186/s13075-017-1497-4</mixed-citation></ref><ref id="B85"><label>85.</label><mixed-citation>Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Time trends in epidemiology and characteristics of psoriatic arthritis over 3 decades: a population-based study. J Rheumatol. 2009;36(2):361–367. doi: 10.3899/jrheum.080691</mixed-citation></ref><ref id="B86"><label>86.</label><mixed-citation>Nossent JC, Gran JT. Epidemiological and clinical characteristics of psoriatic arthritis in northern Norway. Scand J Rheumatol. 2009;38(4):251–255. doi: 10.1080/03009740802609558</mixed-citation></ref><ref id="B87"><label>87.</label><mixed-citation>Egeberg A, Kristensen LE, Thyssen JP, Gislason GH, Gottlieb AB, Coates LC, et al. Incidence and prevalence of psoriatic arthritis in Denmark: a nationwide register linkage study. Ann Rheum Dis. 2017;76(9):1591–1597. doi: 10.1136/annrheumdis-2016-210963</mixed-citation></ref><ref id="B88"><label>88.</label><mixed-citation>Queiro R, Tejón P, Coto P, Alonso S, Alperi M, Sarasqueta C, et al. Clinical differences between men and women with psoriatic arthritis: relevance of the analysis of genes and polymorphisms in the major histocompatibility complex region and of the age at onset of psoriasis. Clin Dev Immunol. 2013;2013:482691. doi: 10.1155/2013/482691</mixed-citation></ref><ref id="B89"><label>89.</label><mixed-citation>Queiro R, Sarasqueta C, Torre JC, Tinturé T, López-Lagunas I. Comparative analysis of psoriatic spondyloarthropathy between men and women. Rheumatol Int. 2001;21(2):66–68. doi: 10.1007/s002960100135</mixed-citation></ref><ref id="B90"><label>90.</label><mixed-citation>Julià A, Tortosa R, Hernanz JM, Cañete JD, Fonseca E, Ferrándiz C, et al. Risk variants for psoriasis vulgaris in a large case-control collection and association with clinical subphenotypes. Hum Mol Genet. 2012;21(20):4549–4557. doi: 10.1093/hmg/dds295</mixed-citation></ref><ref id="B91"><label>91.</label><mixed-citation>Queiro R, Tejón P, Alonso S, Coto P. Age at disease onset: a key factor for understanding psoriatic disease. Rheumatology (Oxford). 2014;53(7):1178–1185. doi: 10.1093/rheumatology/ket363</mixed-citation></ref></ref-list></back></article>
