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<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="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Genes &amp; Cells</journal-id><journal-title-group><journal-title xml:lang="en">Genes &amp; Cells</journal-title><trans-title-group xml:lang="ru"><trans-title>Гены и Клетки</trans-title></trans-title-group><trans-title-group xml:lang="zh"><trans-title>Genes and Cells</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2313-1829</issn><issn publication-format="electronic">2500-2562</issn><publisher><publisher-name xml:lang="en">Human Stem Cells Institute</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">121650</article-id><article-id pub-id-type="doi">10.23868/gc121650</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">Autophagy induction in peripheral blood T-lymphocytes of atopic asthma patients</article-title><trans-title-group xml:lang="ru"><trans-title>Индукция аутофагии в Т-лимфоцитахпериферической крови больных атопическойбронхиальной астмой</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Skibo</surname><given-names>Y V</given-names></name><name xml:lang="ru"><surname>Скибо</surname><given-names>Ю В</given-names></name></name-alternatives><bio xml:lang="en"><p>Kazan (Volga Region) Federal University, Kazan</p></bio><bio xml:lang="ru"><p>Казанский (Приволжский) федеральный университет, Казань</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Ponomareva</surname><given-names>A A</given-names></name><name xml:lang="ru"><surname>Пономарева</surname><given-names>А А</given-names></name></name-alternatives><bio xml:lang="en"><p>Kazan Institute of Biochemistry and Biophysics of RAS, Kazan</p></bio><bio xml:lang="ru"><p>Казанский институт биохимии и биофизики РАН, Казань</p></bio><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Reshetnikova</surname><given-names>I D</given-names></name><name xml:lang="ru"><surname>Решетникова</surname><given-names>И Д</given-names></name></name-alternatives><bio xml:lang="en"><p>Kazan SRI of Epidemiology and Microbiology, Kazan</p></bio><bio xml:lang="ru"><p>Казанский НИИ эпидемиологии и микробиологии, Казань</p></bio><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Abramova</surname><given-names>Z I</given-names></name><name xml:lang="ru"><surname>Абрамова</surname><given-names>З И</given-names></name></name-alternatives><bio xml:lang="en"><p>Kazan (Volga Region) Federal University, Kazan</p></bio><bio xml:lang="ru"><p>Казанский (Приволжский) федеральный университет, Казань</p></bio><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Kazan (Volga Region) Federal University, Kazan</institution></aff><aff><institution xml:lang="ru">Казанский (Приволжский) федеральный университет, Казань</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Kazan Institute of Biochemistry and Biophysics of RAS, Kazan</institution></aff><aff><institution xml:lang="ru">Казанский институт биохимии и биофизики РАН, Казань</institution></aff></aff-alternatives><aff-alternatives id="aff3"><aff><institution xml:lang="en">Kazan SRI of Epidemiology and Microbiology, Kazan</institution></aff><aff><institution xml:lang="ru">Казанский НИИ эпидемиологии и микробиологии, Казань</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2012-09-15" publication-format="electronic"><day>15</day><month>09</month><year>2012</year></pub-date><volume>7</volume><issue>3</issue><issue-title xml:lang="en">NO3 (2012)</issue-title><issue-title xml:lang="ru">№3 (2012)</issue-title><fpage>146</fpage><lpage>150</lpage><history><date date-type="received" iso-8601-date="2023-01-11"><day>11</day><month>01</month><year>2023</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2012, Eco-Vector</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2012, Эко-Вектор</copyright-statement><copyright-year>2012</copyright-year><copyright-holder xml:lang="en">Eco-Vector</copyright-holder><copyright-holder xml:lang="ru">Эко-Вектор</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://genescells.ru/2313-1829/article/view/121650">https://genescells.ru/2313-1829/article/view/121650</self-uri><abstract xml:lang="en"><p>Autophagy is a fundamental process that ensures
the regulation of T-cell homeostasis. In case of apoptosis
induction disruption in the cell it could be single mechanism of
the cell death. Previously was shown inhibition of lymphocyte
apoptosis in patients with bronchial asthma, so the main study
of this work has focused on the study development process
of autophagy in T-lymphocytes of patients with bronchial
asthma. The article presents the main morphological changes
in cells associated with activation of autophagy (formation
autophagosome). In addition to morphological changes in
lymphocytes, we have shown the expression of autophagy
marker protein (LC3B). We found that in T-lymphocytes of
patients with severe asthma are simultaneous activation of
both autophagy and apoptosis, and autophagy is a stimulus
to cell death.</p></abstract><trans-abstract xml:lang="ru"><p>Аутофагия является фундаментальным процессом, который обеспечивает регуляцию гомеостаза Т-лимфоцитов.
Она может являться единственным механизмом гибели
клеток, когда в клетке имеются нарушения в индукции
апоптоза. Ранее было показано торможение апоптоза лимфоцитов больных бронхиальной астмой, поэтому основные
исследования данной работы были направлены на изучение развития процесса аутофагии в Т-лимфоцитах больных
бронхиальной астмой. В статье представлены основные
морфологические изменения клеток, связанные с активацией аутофагии (формирование аутофагосом). Помимо
морфологических изменений лимфоцитов, приводятся результаты исследования экспрессии маркерного белка аутофагии - LC3B. В работе установлено, что в Т-лимфоцитах
больных тяжелой формой астмы происходит одновременная активация как аутофагии, так и апоптоза, и аутофагия
является стимулом к гибели клеток.</p></trans-abstract><kwd-group xml:lang="en"><kwd>autophagy</kwd><kwd>apoptosis</kwd><kwd>T-lymphocytes</kwd><kwd>asthma</kwd><kwd>LC3B protein</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>аутофагия</kwd><kwd>апоптоз</kwd><kwd>Т-лимфоциты</kwd><kwd>астма</kwd><kwd>LC3B белок</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Бростофор Д., Мейл Д., Ройтт А. и др. Иммунология. Мо- сква: Логосфера; 2007.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Jameson S.C. Maintaining the norm: T-cell homeostasis. Nat. Rev. Immunol. 2002; 2: 547-56.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Plas D.R., Rathmell J.C., Thompson C.B. Homeostatic control of lymphocyte survival: potential origins and implications. Nat. Immunol. 2002; 3(6): 515-21.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Blattman J.N., Antia R., Sourdive D.J. et al. Estimating the precursor frequency of naive antigen-specific CD8 T cells. J. Exp. Med. 2002; 195(5): 657-64.</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Badovinac V.P., Harty J.T. Programming, demarcating, and manipulating CD8+ T-cell memory. Immunol. Rev. 2006; 211: 67-80.</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Pua H.H., Dzhagalov I., Chuck M. et al. A critical role for the autophagy gene Atg5 in T cell survival and proliferation. J. Exp. Med. 2007; 204: 25-31.</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Walter M.J., Holtzman M.J. A centennial history of research on asthma pathogenesis. Am. J. Respir. Cell Mol. Biol. 2005; 32: 483-9.</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Бойчук С.В., Мустафин И.Г. Fas-рецептор и его роль при ато- пических заболеваниях. Иммунология 2001; 3: 24-8.</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>O'Sullivan S., Cormican L., Burke C.M. Fluticasone induces T cell apoptosis in the bronchial wall of mild to moderate asthmatics. Asthma 2004; 59(8): 657-61.</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Lockshina R.A., Zakerib Z. Apoptosis, autophagy and more. Int. J. Biochem. Cell B. 2004; 36(12): 2405-19.</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Klionsky D.J. The molecular machinery of autophagy: unanswered questions. Cell Science 2005; 118: 7-18.</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Paglin S., Hollister T., Delohery T. et al. A novel response of cancer cells to radiation involves autophagy and formation of acidic vesicles. Cancer Res. 2001; 61: 439-44.</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Kabeya Y., Mizushima N., Ueno T. et al. LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing. EMBO 2000; 19: 5720-8.</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Li C., Capan E., Zhao Y. et al. Autophagy Is Induced in CD4-T Cells and Important for the Growth Factor-Withdrawal Cell Death. Immunology 2006; 177(8): 5163-8.</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Bursch W. The autophagosomal-lysosomal compartment in programmed cell death. Cell Death Differ. 2001; 8(6): 569-81.</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Edinger A.L., Thompson C.B. Death by design: apoptosis, necrosis and autophagy. Current Opinion in Cell Biology 2004; 16: 663-9.</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Скибо Ю.В., Курмаева Н.Ш. Особенности апоптоза лимфо- цитов у больных легкой и тяжелой атопической бронхиальной аст- мой. Практическая медицина 2012. В печати.</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Скибо Ю.В., Курмаева Н.Ш., Цибулькина В.Н. и др. Струк- тура основных популяций лимфоцитов у больных атопической брон- хиальной астмой разной степени тяжести. Практическая медицина 2012. В печати.</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Kroemer G., Jaattela M. Lysosomes and autophagy in cell death control. Nat. Rev. Cancer. 2005; 5: 886-97.</mixed-citation></ref></ref-list></back></article>
