<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<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">nogr</journal-id><journal-title-group><journal-title xml:lang="ru">Экспериментальная и клиническая гастроэнтерология</journal-title><trans-title-group xml:lang="en"><trans-title>Experimental and Clinical Gastroenterology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1682-8658</issn><publisher><publisher-name>«Global Media Technologies»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.31146/1682-8658-ecg-231-11-81-89</article-id><article-id custom-type="elpub" pub-id-type="custom">nogr-2966</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>КЛИНИЧЕСКАЯ ГАСТРОЭНТЕРОЛОГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL GASTROENTEROLOGY</subject></subj-group></article-categories><title-group><article-title>Содержание Т-лимфоцитов, экспрессирующих эктонуклеотидазы CD39 и СD73, при язвенном колите</article-title><trans-title-group xml:lang="en"><trans-title>Content of T lymphocytes expressing ectonucleotidases CD39 and СD73 in ulcerative colitis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6266-3289</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Жулай</surname><given-names>Г. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Zhulai</surname><given-names>G. A.</given-names></name></name-alternatives><email xlink:type="simple">zhgali-111@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/0000-0001-8697-2086</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Топчиева</surname><given-names>Л. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Topchieva</surname><given-names>L. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.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/0009-0006-2738-3728</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Аторин</surname><given-names>Д. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Atorin</surname><given-names>D. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.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/0000-0003-2613-5694</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Дуданова</surname><given-names>О. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Dudanova</surname><given-names>O. P.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7620-7065</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Курбатова</surname><given-names>И. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurbatova</surname><given-names>I. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Институт биологии - обособленное подразделение ФГБУН «Федеральный исследовательский центр “Карельский научный центр Российской академии наук”»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Institute of Biology, Karelian Research Centre, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБОУ ВО «Петрозаводский государственный университет»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Petrozavodsk State University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>17</day><month>11</month><year>2024</year></pub-date><volume>0</volume><issue>11</issue><fpage>81</fpage><lpage>89</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Жулай Г.А., Топчиева Л.В., Аторин Д.А., Дуданова О.П., Курбатова И.В., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Жулай Г.А., Топчиева Л.В., Аторин Д.А., Дуданова О.П., Курбатова И.В.</copyright-holder><copyright-holder xml:lang="en">Zhulai G.A., Topchieva L.V., Atorin D.A., Dudanova O.P., Kurbatova I.V.</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://www.nogr.org/jour/article/view/2966">https://www.nogr.org/jour/article/view/2966</self-uri><abstract><p>Цель исследования - оценить содержание Т-клеток, экспрессирующих эктонуклеотидазы CD39 и CD73, а также их связь с уровнем мРНК гена ADORA2A, кодирующего аденозиновый рецептор A2A, в периферической крови больных язвенным колитом (ЯК) в сравнении со здоровыми донорами. Материал и методы. Обследована группа больных ЯК (n=18) и здоровых доноров (n=22). Содержание лимфоцитов, несущих на своей поверхности эктонуклеотидазы, в периферической крови оценивали методом проточной цитометрии. Уровень мРНК гена ADORA2A анализировали методом ПЦР в режиме реального времени. Результаты. У пациентов с ЯК регистрировали более высокое содержание активированных CD8+CD25+ Т-клеток, чем у здоровых людей (5,85% (3,02-27,17) против 2,36% (1,35-3,12) при p=0,0008). Экспрессия эктонуклеотидаз на поверхности Т-клеток зависела от их принадлежности к определенной субпопуляции. Отмечено, что у больных ЯК содержание CD8+СD73+ Т-клеток было выше, чем у здоровых лиц (29,29% (19,73-49,70) против 20,00% (8,01-27,41) при р=0,031). Повышение содержания CD8+СD73+ Т-клеток при ЯК сопровождалось повышением числа активированных CD8+CD25+ Т-клеток (rs=0,66, p=0,031). У больных ЯК уровень мРНК ADORA2A выше, чем у здоровых доноров (0,415×103 (0,006×103-1,540×103) против 0,014×103 (0,005×103-0,046×103) при p=0,000025). Уровень мРНК ADORA2A не коррелировал с количеством CD39+ и CD73+ Т-клеток, также как и с содержанием самих CD8+-, CD4+- и Treg-клеток. Заключение. У больных ЯК значимую роль в аденозинэргичном пути могут играть активированные цитотоксические CD8+CD73+ Т-клетки.</p></abstract><trans-abstract xml:lang="en"><p>The aim of the study was to evaluate the content of T-cells expressing ectonucleotidases CD39 and CD73, as well as their association with the mRNA level of ADORA2A gene encoding adenosine A2A receptor in the peripheral blood of ulcerative colitis (UC) patients in comparison with healthy donors. Material and Methods. The group of UC patients (n=18) and healthy donors (n=22) was examined. The content of lymphocytes carrying ectonucleotidases on their surface in peripheral blood was estimated by flow cytometry. The mRNA level of ADORA2A gene was analyzed by real-time PCR. Results. A higher content of activated CD8+CD25+ T-cells was registered in UC patients than in healthy subjects (5.85% (3.02-27.17) vs. 2.36% (1.35-3.12) at p=0.0008). Expression of ectonucleotidases on the surface of T-cells depended on their belonging to a certain subpopulation. It was noted that in UC patients the content of CD8+CD73+ T-cells was higher than in healthy individuals (29.29% (19.73-49.70) vs. 20.00% (8.01-27.41) at p=0.031). The increase in CD8+CD73+ T-cells in UC was accompanied by an increase in the number of activated CD8+CD25+ T-cells (rs=0.66, p=0.031). The level of ADORA2A mRNA was higher in UC patients than in healthy donors (0.415×103 (0.006×103-1.540×103) vs. 0.014×103 (0.005×103-0.046×103) at p=0.000025). ADORA2A mRNA levels did not correlate with the number of CD39+ and CD73+ T cells, nor did they correlate with the content of CD8+, CD4+ and Treg cells themselves. Conclusion. In UC patients, activated cytotoxic CD8+CD73+ T cells may play a significant role in the adenosineergic pathway.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>Т-клетки</kwd><kwd>CD39</kwd><kwd>CD73</kwd><kwd>язвенный колит</kwd><kwd>ген ADORA2A</kwd></kwd-group><kwd-group xml:lang="en"><kwd>T cells</kwd><kwd>CD39</kwd><kwd>CD73</kwd><kwd>ulcerative colitis</kwd><kwd>ADORA2A gene</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">Shelygin Yu.A., Ivashkin V.T., Belousova E.A. et al. Ulcerative colitis (K51), adults. Koloproktologiâ. 2023;22(1):10-44. (In Russ) doi: 10.33878/2073-7556-2023-22-1-10-44.</mixed-citation><mixed-citation xml:lang="en">Shelygin Yu.A., Ivashkin V.T., Belousova E.A. et al. Ulcerative colitis (K51), adults. Koloproktologiâ. 2023;22(1):10-44. (In Russ) doi: 10.33878/2073-7556-2023-22-1-10-44.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Antonioli L., Fornai M., Pellegrini C., Bertani L., Nemeth Z.H., Blandizzi C. Inflammatory Bowel Diseases: It’s Time for the Adenosine System. Front Immunol. 2020;11:1310. doi: 10.3389/fimmu.2020.01310.</mixed-citation><mixed-citation xml:lang="en">Antonioli L., Fornai M., Pellegrini C., Bertani L., Nemeth Z.H., Blandizzi C. Inflammatory Bowel Diseases: It’s Time for the Adenosine System. Front Immunol. 2020;11:1310. doi: 10.3389/fimmu.2020.01310.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Pasquini S., Contri C., Borea P.A., Vincenzi F., Varani K. Adenosine and Inflammation: Here, There and Everywhere. IJMS. 2021;22(14):7685. doi: 10.3390/ijms22147685.</mixed-citation><mixed-citation xml:lang="en">Pasquini S., Contri C., Borea P.A., Vincenzi F., Varani K. Adenosine and Inflammation: Here, There and Everywhere. IJMS. 2021;22(14):7685. doi: 10.3390/ijms22147685.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Ohta A., Sitkovsky M. Extracellular Adenosine-Mediated Modulation of Regulatory T Cells. Front Immunol. 2014;5. doi: 10.3389/fimmu.2014.00304.</mixed-citation><mixed-citation xml:lang="en">Ohta A., Sitkovsky M. Extracellular Adenosine-Mediated Modulation of Regulatory T Cells. Front Immunol. 2014;5. doi: 10.3389/fimmu.2014.00304.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu Y., Zhuang Z., Wu Q. et al. CD39/CD73/A2a Adenosine Metabolic Pathway: Targets for Moxibustion in Treating DSS-Induced Ulcerative Colitis. Am J Chin Med. 2021;49(03):661-676. doi: 10.1142/S0192415X21500300.</mixed-citation><mixed-citation xml:lang="en">Zhu Y., Zhuang Z., Wu Q. et al. CD39/CD73/A2a Adenosine Metabolic Pathway: Targets for Moxibustion in Treating DSS-Induced Ulcerative Colitis. Am J Chin Med. 2021;49(03):661-676. doi: 10.1142/S0192415X21500300.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Kim S.E., Ko I.G., Jin J.J. et al. Polydeoxyribonucleotide Exerts Therapeutic Effect by Increasing VEGF and Inhibiting Inflammatory Cytokines in Ischemic Colitis Rats. BioMed Research International. 2020;2020:1-11. doi: 10.1155/2020/2169083.</mixed-citation><mixed-citation xml:lang="en">Kim S.E., Ko I.G., Jin J.J. et al. Polydeoxyribonucleotide Exerts Therapeutic Effect by Increasing VEGF and Inhibiting Inflammatory Cytokines in Ischemic Colitis Rats. BioMed Research International. 2020;2020:1-11. doi: 10.1155/2020/2169083.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Bahreyni A., Samani S.S., Khazaei M., Ryzhikov M., Avan A., Hassanian S.M. Therapeutic potentials of adenosine receptors agonists and antagonists in colitis; Current status and perspectives. Journal Cellular Physiology. 2018;233(4):2733-2740. doi: 10.1002/jcp.26073.</mixed-citation><mixed-citation xml:lang="en">Bahreyni A., Samani S.S., Khazaei M., Ryzhikov M., Avan A., Hassanian S.M. Therapeutic potentials of adenosine receptors agonists and antagonists in colitis; Current status and perspectives. Journal Cellular Physiology. 2018;233(4):2733-2740. doi: 10.1002/jcp.26073.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Beyazit Y., Koklu S., Tas A. et al. Serum adenosine deaminase activity as a predictor of disease severity in ulcerative colitis. Journal of Crohn’s and Colitis. 2012;6(1):102-107. doi: 10.1016/j.crohns.2011.07.010.</mixed-citation><mixed-citation xml:lang="en">Beyazit Y., Koklu S., Tas A. et al. Serum adenosine deaminase activity as a predictor of disease severity in ulcerative colitis. Journal of Crohn’s and Colitis. 2012;6(1):102-107. doi: 10.1016/j.crohns.2011.07.010.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Dal Ben D., Antonioli L., Lambertucci C., Fornai M., Blandizzi C., Volpini R. Purinergic Ligands as Potential Therapeutic Tools for the Treatment of Inflammation-Related Intestinal Diseases. Front Pharmacol. 2018;9:212. doi: 10.3389/fphar.2018.00212.</mixed-citation><mixed-citation xml:lang="en">Dal Ben D., Antonioli L., Lambertucci C., Fornai M., Blandizzi C., Volpini R. Purinergic Ligands as Potential Therapeutic Tools for the Treatment of Inflammation-Related Intestinal Diseases. Front Pharmacol. 2018;9:212. doi: 10.3389/fphar.2018.00212.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Ercan G., Yigitturk G., Erbas O. Therapeutic effect of adenosine on experimentally induced acute ulcerative colitis model in rats. Acta Cir Bras. 2019;34(12): e201901204. doi: 10.1590/s0102-865020190120000004.</mixed-citation><mixed-citation xml:lang="en">Ercan G., Yigitturk G., Erbas O. Therapeutic effect of adenosine on experimentally induced acute ulcerative colitis model in rats. Acta Cir Bras. 2019;34(12): e201901204. doi: 10.1590/s0102-865020190120000004.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Rybaczyk L., Rozmiarek A., Circle K. et al. New bioinformatics approach to analyze gene expressions and signaling pathways reveals unique purine gene dysregulation profiles that distinguish between CD and UC: Inflammatory Bowel Diseases. 2009;15(7):971-984. doi: 10.1002/ibd.20893.</mixed-citation><mixed-citation xml:lang="en">Rybaczyk L., Rozmiarek A., Circle K. et al. New bioinformatics approach to analyze gene expressions and signaling pathways reveals unique purine gene dysregulation profiles that distinguish between CD and UC: Inflammatory Bowel Diseases. 2009;15(7):971-984. doi: 10.1002/ibd.20893.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Ye J.H., Rajendran V.M. Adenosine: An immune modulator of inflammatory bowel diseases. WJG. 2009;15(36):4491. doi: 10.3748/wjg.15.4491.</mixed-citation><mixed-citation xml:lang="en">Ye J.H., Rajendran V.M. Adenosine: An immune modulator of inflammatory bowel diseases. WJG. 2009;15(36):4491. doi: 10.3748/wjg.15.4491.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Künzli B.M., Berberat P.O., Dwyer K. et al. Variable impact of CD39 in experimental murine colitis. Dig Dis Sci. 2011; 56: 1393-1403. doi: 10.1007/s10620-010-1425-9.</mixed-citation><mixed-citation xml:lang="en">Künzli B.M., Berberat P.O., Dwyer K. et al. Variable impact of CD39 in experimental murine colitis. Dig Dis Sci. 2011; 56: 1393-1403. doi: 10.1007/s10620-010-1425-9.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Friedman D.J., Künzli B.M., A-Rahim Y.I., Sevigny J., Berberat P.O., Enjyoji K. et al. CD39 deletion exacerbates experimental murine colitis and human polymorphisms increase susceptibility to inflammatory bowel disease. Proceedings of the National Academy of Sciences. 2009;106(39):16788-16793. doi: 10.1073/pnas.0902869106.</mixed-citation><mixed-citation xml:lang="en">Friedman D.J., Künzli B.M., A-Rahim Y.I., Sevigny J., Berberat P.O., Enjyoji K. et al. CD39 deletion exacerbates experimental murine colitis and human polymorphisms increase susceptibility to inflammatory bowel disease. Proceedings of the National Academy of Sciences. 2009;106(39):16788-16793. doi: 10.1073/pnas.0902869106.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Longhi M.S., Moss A., Jiang Z.G., Robson S.C. Purinergic signaling during intestinal inflammation. J Mol Med. 2017;95(9):915-925. doi: 10.1007/s00109-017-1545-1.</mixed-citation><mixed-citation xml:lang="en">Longhi M.S., Moss A., Jiang Z.G., Robson S.C. Purinergic signaling during intestinal inflammation. J Mol Med. 2017;95(9):915-925. doi: 10.1007/s00109-017-1545-1.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Ye H., Zhao J., Xu X., Zhang D., Shen H., Wang S. Role of adenosine A2a receptor in cancers and autoimmune diseases. Immunity Inflam &amp; Disease. 2023;11(4): e826. doi: 10.1002/iid3.826.</mixed-citation><mixed-citation xml:lang="en">Ye H., Zhao J., Xu X., Zhang D., Shen H., Wang S. Role of adenosine A2a receptor in cancers and autoimmune diseases. Immunity Inflam &amp; Disease. 2023;11(4): e826. doi: 10.1002/iid3.826.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Borsellino G., Kleinewietfeld M., Di Mitri D. et al. Expression of ectonucleotidase CD39 by Foxp3+ Treg cells: hydrolysis of extracellular ATP and immune suppression. Blood. 2007;110(4):1225-1232. doi: 10.1182/blood-2006-12-064527.</mixed-citation><mixed-citation xml:lang="en">Borsellino G., Kleinewietfeld M., Di Mitri D. et al. Expression of ectonucleotidase CD39 by Foxp3+ Treg cells: hydrolysis of extracellular ATP and immune suppression. Blood. 2007;110(4):1225-1232. doi: 10.1182/blood-2006-12-064527.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Gibson D.J., Elliott L., McDermott E. et al. Heightened Expression of CD39 by Regulatory T Lymphocytes Is Associated with Therapeutic Remission in Inflammatory Bowel Disease. Inflammatory Bowel Diseases. 2015;21(12):2806-2814. doi: 10.1097/MIB. 0000000000000566.</mixed-citation><mixed-citation xml:lang="en">Gibson D.J., Elliott L., McDermott E. et al. Heightened Expression of CD39 by Regulatory T Lymphocytes Is Associated with Therapeutic Remission in Inflammatory Bowel Disease. Inflammatory Bowel Diseases. 2015;21(12):2806-2814. doi: 10.1097/MIB. 0000000000000566.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Radygina T.V., Petrichuk S.V., Kuptsova D.G. et al. Content of CD4+ cells expressing CD39/CD73 ectonucleotidases in children with inflammatory bowel diseases. Bulletin of RSMU. 2022; (4): 17-23. doi: 10.24075/brsmu.2022.039.</mixed-citation><mixed-citation xml:lang="en">Radygina T.V., Petrichuk S.V., Kuptsova D.G. et al. Content of CD4+ cells expressing CD39/CD73 ectonucleotidases in children with inflammatory bowel diseases. Bulletin of RSMU. 2022; (4): 17-23. doi: 10.24075/brsmu.2022.039.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Lord J.D., Shows D.M., Chen J., Thirlby R.C. Human Blood and Mucosal Regulatory T Cells Express Activation Markers and Inhibitory Receptors in Inflammatory Bowel Disease. Unutmaz D, ed. PLoS ONE. 2015;10(8): e0136485. doi: 10.1371/journal.pone.0136485.</mixed-citation><mixed-citation xml:lang="en">Lord J.D., Shows D.M., Chen J., Thirlby R.C. Human Blood and Mucosal Regulatory T Cells Express Activation Markers and Inhibitory Receptors in Inflammatory Bowel Disease. Unutmaz D, ed. PLoS ONE. 2015;10(8): e0136485. doi: 10.1371/journal.pone.0136485.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Longhi M.S., Moss A., Bai A. et al. Characterization of Human CD39+ Th17 Cells with Suppressor Activity and Modulation in Inflammatory Bowel Disease. Hogan SP, ed. PLoS ONE. 2014;9(2): e87956. doi: 10.1371/journal.pone.0087956.</mixed-citation><mixed-citation xml:lang="en">Longhi M.S., Moss A., Bai A. et al. Characterization of Human CD39+ Th17 Cells with Suppressor Activity and Modulation in Inflammatory Bowel Disease. Hogan SP, ed. PLoS ONE. 2014;9(2): e87956. doi: 10.1371/journal.pone.0087956.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Libera J., Wittner M., Kantowski M. et al. Decreased Frequency of Intestinal CD39+γδ+ T Cells With Tissue-Resident Memory Phenotype in Inflammatory Bowel Disease. Front Immunol. 2020;11:567472. doi: 10.3389/fimmu.2020.567472.</mixed-citation><mixed-citation xml:lang="en">Libera J., Wittner M., Kantowski M. et al. Decreased Frequency of Intestinal CD39+γδ+ T Cells With Tissue-Resident Memory Phenotype in Inflammatory Bowel Disease. Front Immunol. 2020;11:567472. doi: 10.3389/fimmu.2020.567472.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Ferretti E., Horenstein A.L., Canzonetta C., Costa F., Morandi F. Canonical and non-canonical adenosinergic pathways. Immunology Letters. 2019;205:25-30. doi: 10.1016/j.imlet.2018.03.007.</mixed-citation><mixed-citation xml:lang="en">Ferretti E., Horenstein A.L., Canzonetta C., Costa F., Morandi F. Canonical and non-canonical adenosinergic pathways. Immunology Letters. 2019;205:25-30. doi: 10.1016/j.imlet.2018.03.007.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Wang R., Wang Y., Wu C. et al. CD73 blockade alleviates intestinal inflammatory responses by regulating macrophage differentiation in ulcerative colitis. Exp Ther Med. 2023;25(6):272. doi: 10.3892/etm.2023.11972.</mixed-citation><mixed-citation xml:lang="en">Wang R., Wang Y., Wu C. et al. CD73 blockade alleviates intestinal inflammatory responses by regulating macrophage differentiation in ulcerative colitis. Exp Ther Med. 2023;25(6):272. doi: 10.3892/etm.2023.11972.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Doherty G.A., Bai A., Hanidziar D. et al. CD 73 is a phenotypic marker of effector memory T h17 cells in inflammatory bowel disease. Eur J Immunol. 2012;42(11):3062-3072. doi: 10.1002/eji.201242623.</mixed-citation><mixed-citation xml:lang="en">Doherty G.A., Bai A., Hanidziar D. et al. CD 73 is a phenotypic marker of effector memory T h17 cells in inflammatory bowel disease. Eur J Immunol. 2012;42(11):3062-3072. doi: 10.1002/eji.201242623.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Ohta A., Ohta A., Madasu M. et al. A2A Adenosine Receptor May Allow Expansion of T Cells Lacking Effector Functions in Extracellular Adenosine-Rich Microenvironments. The Journal of Immunology. 2009;183(9):5487-5493. doi: 10.4049/jimmunol.0901247.</mixed-citation><mixed-citation xml:lang="en">Ohta A., Ohta A., Madasu M. et al. A2A Adenosine Receptor May Allow Expansion of T Cells Lacking Effector Functions in Extracellular Adenosine-Rich Microenvironments. The Journal of Immunology. 2009;183(9):5487-5493. doi: 10.4049/jimmunol.0901247.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Vuerich M., Nguyen D.H., Ferrari D., Longhi M.S. Adenosine-mediated immune responses in inflammatory bowel disease. Front Cell Dev Biol. 2024;12:1429736. doi: 10.3389/fcell.2024.1429736.</mixed-citation><mixed-citation xml:lang="en">Vuerich M., Nguyen D.H., Ferrari D., Longhi M.S. Adenosine-mediated immune responses in inflammatory bowel disease. Front Cell Dev Biol. 2024;12:1429736. doi: 10.3389/fcell.2024.1429736.</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>
