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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="en"><front><journal-meta><journal-id journal-id-type="publisher-id">sechenov</journal-id><journal-title-group><journal-title xml:lang="en">Sechenov Medical Journal</journal-title><trans-title-group xml:lang="ru"><trans-title>Сеченовский вестник</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2218-7332</issn><issn pub-type="epub">2658-3348</issn><publisher><publisher-name>Сеченовский Университет</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">sechenov-803</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="en"><subject>THE ACHIEVEMENTS OF MODERN PATHOPHYSIOLOGY</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ДОСТИЖЕНИЯ СОВРЕМЕННОЙ ПАТОФИЗИОЛОГИИ</subject></subj-group></article-categories><title-group><article-title>Opportunities for management of macrophage phenotype reprogramming</article-title><trans-title-group xml:lang="ru"><trans-title>Возможности управления процессом перепрограммирования фенотипа макрофагов</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сахаров</surname><given-names>В. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Sakharov</surname><given-names>V. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант</p></bio><bio xml:lang="en"><p>post-graduate</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Литвицкий</surname><given-names>П. Ф.</given-names></name><name name-style="western" xml:lang="en"><surname>Litvitsky</surname><given-names>P. F.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Пeтр Францевич Литвицкий, д.м.н., чл.-корр. РАН, профессор, заведующий кафедрой патофизиологии</p><p>119991, г. Москва, ул. Трубецкая, д. 8, стр. 2</p><p>8 (985) 769–07–38</p></bio><bio xml:lang="en"><p>Petr Frantsevich Litvitsky, MD, corresp. member of RAS, prof., head of the chair of pathophysiology</p><p>8/2 Trubetskaya str., Moscow, 119991</p><p>8 (985) 769–07–38</p></bio><email xlink:type="simple">litvicki@mma.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Первый МГМУ им. И.М. Сеченова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>I.M. Sechenov First MSMU</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2014</year></pub-date><pub-date pub-type="epub"><day>30</day><month>12</month><year>2014</year></pub-date><volume>0</volume><issue>4</issue><fpage>89</fpage><lpage>96</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Sakharov V.N., Litvitsky P.F., 2014</copyright-statement><copyright-year>2014</copyright-year><copyright-holder xml:lang="ru">Сахаров В.Н., Литвицкий П.Ф.</copyright-holder><copyright-holder xml:lang="en">Sakharov V.N., Litvitsky P.F.</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.sechenovmedj.com/jour/article/view/803">https://www.sechenovmedj.com/jour/article/view/803</self-uri><abstract><p>This article reviews the recent literature on opportunities for reprogramming of macrophage phenotypes. Much attention is devoted to the stimulus, signal pathways and its effects as well as some regulational mechanisms.</p></abstract><trans-abstract xml:lang="ru"><p>Представлен обзор литературы последних лет о возможностях целенаправленного перепрограммирования фенотипа активированных макрофагов. Основное внимание уделено характеристике индукторов их активации, реализации сигнальных путей и их эффектов, а также механизмов их регуляции.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>активация макрофагов</kwd><kwd>цитокины</kwd><kwd>воспаление</kwd></kwd-group><kwd-group xml:lang="en"><kwd>macrophage activation</kwd><kwd>cytokines</kwd><kwd>inflammation</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">Martinez F.O., Gordon. S. The M1 and M2 paradigm of macrophage activation: time for reassessment // F1000Prime Reports. 2014. Vol. 6. № 13. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944738/ (дата обращения: 05.04.2014).</mixed-citation><mixed-citation xml:lang="en">Martinez F.O., Gordon. S. The M1 and M2 paradigm of macrophage activation: time for reassessment // F1000Prime Reports. 2014. Vol. 6. № 13. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944738/ (дата обращения: 05.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Edwards J.P., Zhang X., Frauwirth K.A., Mosser D.M. Biochemical and functional characterization of three activated macrophage populations // J. Leukoc. Biol. 2006. Vol. 80. № 6. P. 1298–1307. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2642590/ (дата обращения: 15.04.2014).</mixed-citation><mixed-citation xml:lang="en">Edwards J.P., Zhang X., Frauwirth K.A., Mosser D.M. Biochemical and functional characterization of three activated macrophage populations // J. Leukoc. Biol. 2006. Vol. 80. № 6. P. 1298–1307. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2642590/ (дата обращения: 15.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Лямина С.В., Веденикин Т.Ю., Круглов С.В. и др. Особенности фагоцитарной и миграционной активности альвеолярных макрофагов М1 и М2 фенотипов // Фундаментальные исследования. 2011. № 11 (ч. 3). С. 536–539. URL: http://www.rae.ru/fs/?section=content&amp;op=show_article&amp;article_id=7981832 (дата обращения: 15.04.2014).</mixed-citation><mixed-citation xml:lang="en">Lyamina S.V., Vedenikin T.Yu., Kruglov S.V. et al. Characteristics of phagocytic and migration activity of alveolar macrophages of M1 and M2 phenotypes // Fundamentalnye issledovaniya. 2011; 11(3): 536–539. URL: http://www.rae.ru/fs/?section=content&amp;op=show_article&amp;article_id=7981832 (date accessed: 15.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu M., John S., Berg M., Leonard W.J. Functional association of Nmi with Stat5 and Stat1 in IL-2- and IFNgamma-mediated signaling // Cell. 1999. № 96(1). P. 121-130. URL: http://www.ncbi.nlm.nih.gov/pubmed/9989503 (дата обращения: 22.08.2014).</mixed-citation><mixed-citation xml:lang="en">Zhu M., John S., Berg M., Leonard W.J. Functional association of Nmi with Stat5 and Stat1 in IL-2- and IFNgamma-mediated signaling // Cell. 1999. № 96(1). P. 121-130. URL: http://www.ncbi.nlm.nih.gov/pubmed/9989503 (дата обращения: 22.08.2014).</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Whyte C.S., Bishop E.T., Ruckerl D. et al. Suppressor of cytokine signaling (SOCS)1 is a key determinant of differential macrophage activation and function // J. Leukoc. Biol. 2011. № 90. P. 845–854. URL: http://m.jleukbio.org/content/90/5/845.full.pdf+html (дата обращения: 17.04.2014).</mixed-citation><mixed-citation xml:lang="en">Whyte C.S., Bishop E.T., Ruckerl D. et al. Suppressor of cytokine signaling (SOCS)1 is a key determinant of differential macrophage activation and function // J. Leukoc. Biol. 2011. № 90. P. 845–854. URL: http://m.jleukbio.org/content/90/5/845.full.pdf+html (дата обращения: 17.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Van Dyken S.J., Locksley R.M. Interleukin-4- and interleukin-13-mediated alternatively activated macrophages: roles in homeostasis and disease // Ann. Rev. Immunol. 2013. № 31. P. 317–343. http://http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3606684/ (дата обращения: 15.04.2014).</mixed-citation><mixed-citation xml:lang="en">Van Dyken S.J., Locksley R.M. Interleukin-4- and interleukin-13-mediated alternatively activated macrophages: roles in homeostasis and disease // Ann. Rev. Immunol. 2013. № 31. P. 317–343. http://http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3606684/ (дата обращения: 15.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Verstak B., Nagpal K., Bottomley S.P. et al. MyD88 adapterlike (Mal)/TIRAP interaction with TRAF6 is critical for TLR2- and TLR4-mediated NF-kappaB proinfl ammatory responses // J. Biol. Chem. 2009. № 284(36). P. 24192–24203. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782013/ (дата обращения: 22.08.2014).</mixed-citation><mixed-citation xml:lang="en">Verstak B., Nagpal K., Bottomley S.P. et al. MyD88 adapterlike (Mal)/TIRAP interaction with TRAF6 is critical for TLR2- and TLR4-mediated NF-kappaB proinfl ammatory responses // J. Biol. Chem. 2009. № 284(36). P. 24192–24203. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782013/ (дата обращения: 22.08.2014).</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Reim D., Rossmann-Bloeck T., Jusek G. et al. Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response // J. Leukoc. Biol. 2011. № 90. P. 613–620 URL: http://www.jleukbio.org/content/90/3/613.full (дата обращения: 17.04.2014).</mixed-citation><mixed-citation xml:lang="en">Reim D., Rossmann-Bloeck T., Jusek G. et al. Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response // J. Leukoc. Biol. 2011. № 90. P. 613–620 URL: http://www.jleukbio.org/content/90/3/613.full (дата обращения: 17.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Li S.N., Wang W., Fu S.P. et al. IL-21 modulates release of proinfl ammatory cytokines in LPS-stimulated macrophages through distinct signaling pathways // Mediators of Infl ammation. Vol. 2013. Article ID 548073. 12 p. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888770/ (дата обращения:16.04.2014).</mixed-citation><mixed-citation xml:lang="en">Li S.N., Wang W., Fu S.P. et al. IL-21 modulates release of proinfl ammatory cytokines in LPS-stimulated macrophages through distinct signaling pathways // Mediators of Infl ammation. Vol. 2013. Article ID 548073. 12 p. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888770/ (дата обращения:16.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Xu H., Zhu J., Smith S. et al. Notch-RBP-J signaling regulates IRF8 to promote infl ammatory macrophage polarization // Nat. Immunol. 2012. Vol. 13. № 7. P. 642–650. URL: http://www.ncbi.nlm.nih.gov/pubmed/22610140 (дата обращения: 02.05.2014).</mixed-citation><mixed-citation xml:lang="en">Xu H., Zhu J., Smith S. et al. Notch-RBP-J signaling regulates IRF8 to promote infl ammatory macrophage polarization // Nat. Immunol. 2012. Vol. 13. № 7. P. 642–650. URL: http://www.ncbi.nlm.nih.gov/pubmed/22610140 (дата обращения: 02.05.2014).</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Shi Y., Liu C.H., Roberts A.I. et al. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and T-cell responses: what we do and don't know // Cell Res. 2006. 16(2). P. 126–133. URL: http://www.nature.com/cr/journal/v16/n2/full/7310017a.html (дата обращения: 22.08.2014).</mixed-citation><mixed-citation xml:lang="en">Shi Y., Liu C.H., Roberts A.I. et al. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and T-cell responses: what we do and don't know // Cell Res. 2006. 16(2). P. 126–133. URL: http://www.nature.com/cr/journal/v16/n2/full/7310017a.html (дата обращения: 22.08.2014).</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Iyer S.S., Cheng G. Role of interleukin 10 transcriptional regulation in infl ammation and autoimmune disease // Crit. Rev. Immunol. 2012. № 32(1). P. 23–63. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410706/ (дата обращения: 23.08.2014).</mixed-citation><mixed-citation xml:lang="en">Iyer S.S., Cheng G. Role of interleukin 10 transcriptional regulation in infl ammation and autoimmune disease // Crit. Rev. Immunol. 2012. № 32(1). P. 23–63. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410706/ (дата обращения: 23.08.2014).</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Arnold C.E., Whyte C.S., Gordon P. et al. A critical role for suppressor of cytokine signaling 3 in promoting M1 macrophage activation and function in vitro and in vivo //Immunology. 2013. № 141. P. 96–110. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893853/ (дата обращения: 09.04.2014).</mixed-citation><mixed-citation xml:lang="en">Arnold C.E., Whyte C.S., Gordon P. et al. A critical role for suppressor of cytokine signaling 3 in promoting M1 macrophage activation and function in vitro and in vivo //Immunology. 2013. № 141. P. 96–110. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3893853/ (дата обращения: 09.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">McCall C.E., El Gazzar M., Liu T. et al. Epigenetics, bioenergetics, and microRNA coordinate gene-specifi c reprogramming during acute systemic infl ammation // J. Leukoc. Biol. 2011. № 90. P. 439–446. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157901 (дата обращения: 17.04.2014).</mixed-citation><mixed-citation xml:lang="en">McCall C.E., El Gazzar M., Liu T. et al. Epigenetics, bioenergetics, and microRNA coordinate gene-specifi c reprogramming during acute systemic infl ammation // J. Leukoc. Biol. 2011. № 90. P. 439–446. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3157901 (дата обращения: 17.04.2014).</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Chen C.H., Wang C.Z., Wang Y.H. et al. Eff ects of lowlevel laser therapy on M1-related cytokine expression in monocytes via histone modifi cation // Mediators of Infl ammation. Vol. 2014. Article ID 625048. 13 p. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945284/ (дата обращения: 15.04.2014).</mixed-citation><mixed-citation xml:lang="en">Chen C.H., Wang C.Z., Wang Y.H. et al. Eff ects of lowlevel laser therapy on M1-related cytokine expression in monocytes via histone modifi cation // Mediators of Infl ammation. Vol. 2014. Article ID 625048. 13 p. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945284/ (дата обращения: 15.04.2014).</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>
