РОЛЬ ОТДЕЛЬНЫХ СУБПОПУЛЯЦИЙ CD4+ Т-ЛИМФОЦИТОВ В ПАТОГЕНЕЗЕ ВИЧ-ИНФЕКЦИИ

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Опубликован: дек 8, 2020
Ключевые слова:
ВИЧ-инфекция CD4 Т-клетки наивные Т-лимфоциты Т-клетки центральной памяти Т-клетки эф-фекторной памяти стволовые Т-клетки памяти антиретровирусная терапия

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Евгения Владимировна Сайдакова
ФГБОУВО «Пермский государственный национальный исследовательский университет»
http://orcid.org/0000-0002-4342-5362

Аннотация

Пул CD4+ Т-лимфоцитов состоит из клеток различной степени зрелости. Наивные CD4+ Т-лимфоциты, стволовые CD4+ Т-клетки памяти, CD4+ Т-лимфоциты центральной и эффекторной памяти выполняют различные функции в поддержании гомеостаза иммунной системы. Несмотря на фенотипические различия, клетки каждой из этих субпопуляций могут быть инфицированы ВИЧ. При этом особенности CD4+ Т-лимфоцитов разной степени зрелости определяют роль этих клеток в патогенезе ВИЧ-инфекции. По изменению субпопуляционного состава периферических CD4+ Т-лимфоцитов ВИЧ-инфицированных больных можно судить о степени пораженности иммунной системы, а также делать прогнозы эффективности ее восстановления при назначении высокоактивной антиретровирусной терапии. В статье систематизированы основные события, происходящие с CD4+ Т-клетками различной степени зрелости в условиях неконтролируемого течения ВИЧ-инфекции и на фоне антиретровирусной терапии.

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Как цитировать
Сайдакова, Е. В. (2020). РОЛЬ ОТДЕЛЬНЫХ СУБПОПУЛЯЦИЙ CD4+ Т-ЛИМФОЦИТОВ В ПАТОГЕНЕЗЕ ВИЧ-ИНФЕКЦИИ. Вестник Пермского университета. Серия Биология, (3), 236–246. извлечено от http://press.psu.ru/index.php/bio/article/view/3944
Выпуск
№ 3 (2020): Вестник Пермского университета. Серия Биология. №3. 2020
Раздел
Иммунология

Лицензионный договор на право использования научного произведения в научных журналах, учредителем которых является Пермский государственный национальный исследовательский университет

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Биография автора

Евгения Владимировна Сайдакова, ФГБОУВО «Пермский государственный национальный исследовательский университет»

Кандидат биологических наук, доцент кафедры микробиологии и иммунологии

Библиографические ссылки

Abbas A.K., Murphy K.M., Sher A. Functional diversity of helper T lymphocytes // Nature. 1996. Vol. 383. P. 787‒793.

Abram M.E. et al. Nature, position, and frequency of mutations made in a single cycle of HIV-1 replication // J. Virol. 2010. Vol. 84. P. 9864‒9878.

Appay V., Kelleher A.D. Immune activation and immune aging in HIV infection // Curr Opin HIV AIDS. 2016. Vol. 11. P. 242‒249.

Barre-Sinoussi F. et al. Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS) // Science. 1983. Vol. 220. P. 868‒871.

Bazdar D.A., Sieg S.F., Interleukin-7 enhances proliferation responses to T-cell receptor stimulation in naive CD4+ T cells from human immunodeficiency virus-infected persons // J. Virol. 2007. Vol. 81. P. 12670‒12674.

Breton G. et al. Programmed death-1 is a marker for abnormal distribution of naive/memory T cell subsets in HIV-1 infection // J. Immunol. 2013. Vol. 191. P. 2194‒2204.

Buzon M.J. et al. HIV-1 persistence in CD4+ T cells with stem cell-like properties // Nat. Med. 2014. Vol. 20, P. 139‒142.

Calascibetta F. et al. Antiretroviral Therapy in Simian Immunodeficiency Virus-Infected Sooty Mangabeys: Implications for AIDS Pathogenesis // J. Virol. 2016. Vol. 90. P. 7541‒7551.

Cartwright E.K. et al. Divergent CD4+ T memory stem cell dynamics in pathogenic and nonpathogenic simian immunodeficiency virus infections // J. Immunol. 2014. Vol. 192. P. 4666‒4673.

Case K. Nomenclature: human immunodeficiency virus // Ann. Intern. Med. 1986. Vol. 105. P. 133.

Centers for Disease C. Kaposi's sarcoma and Pneumocystis pneumonia among homosexual men--New York City and California // MMWR Morb. Mortal. Wkly Rep. 1981a. Vol. 30. P. 305‒308.

Centers for Disease C. Pneumocystis pneumonia--Los Angeles // MMWR Morb. Mortal. Wkly Rep. 1981b. Vol. 30. P. 250‒252.

Centers for Disease C. Update on acquired immune deficiency syndrome (AIDS)--United States // MMWR Morb. Mortal. Wkly Rep. 1982. Vol. 31. P. 507‒508, 513‒514.

Chomont N. et al. HIV reservoir size and persistence are driven by T cell survival and homeostatic proliferation // Nat. Med. 2009. Vol. 15, P. 893‒900.

Deng H. et al. Identification of a major co-receptor for primary isolates of HIV-1 // Nature. 1996. Vol. 381, P. 661‒666.

Di Mascio M. et al. Naive T-cell dynamics in human immunodeficiency virus type 1 infection: effects of highly active antiretroviral therapy provide insights into the mechanisms of naive T-cell depletion // J. Virol. 2006. Vol. 80, P. 2665‒2674.

Douek D.C. et al. Changes in thymic function with age and during the treatment of HIV infection // Nature. 1998. Vol. 396. P. 690‒695.

Franzese O. et al. Telomerase activity, hTERT expression, and phosphorylation are downre-gulated in CD4(+) T lymphocytes infected with human immunodeficiency virus type 1 (HIV-1) // J. Med. Virol. 2007. Vol. 79. P. 639‒646.

Gallo R.C. et al. Isolation of human T-cell leukemia virus in acquired immune deficiency syndrome (AIDS) // Science. 1983. Vol. 220. P. 865‒867.

Gange R.W., Jones E.W. Kaposi's sarcoma and immunosuppressive therapy: an appraisal // Clin. Exp. Dermatol. 1978. Vol. 3. P. 135‒146.

Gattinoni L. et al. A human memory T cell subset with stem cell-like properties // Nat. Med. 2011. Vol. 17. P. 1290‒1297.

Groot F. et al. Differential susceptibility of naive, central memory and effector memory T cells to dendritic cell-mediated HIV-1 transmission // Retrovirology. 2006. Vol. 3. P. 52.

Harrington L.E. et al. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages // Nat. Immunol. 2005. Vol. 6. P. 1123‒1132.

Haverkos H.W., Curran J.W. The Current Outbreak of Kaposi's Sarcoma and Opportunistic Infections // CA: A Cancer Journal for Clinicians. 1982. Vol. 32, P. 330‒339.

Hazenberg M.D. et al. Increased cell division but not thymic dysfunction rapidly affects the T-cell receptor excision circle content of the naive T cell population in HIV-1 infection // Nat. Med. 2000. Vol. 6. P. 1036‒1042.

Hersh E.M. et al. Leukocyte subset analysis and related immunological findings in acquired immunodeficiency disease syndrome (AIDS) and malignancies // Diagn. Immunol. 1983. Vol. 1. P. 168‒173.

Imamichi H. et al. Lifespan of effector memory CD4+ T cells determined by replication-incompetent integrated HIV-1 provirus // AIDS. 2014. Vol. 28. P. 1091‒1099.

Klatt N.R. et al. Limited HIV infection of central memory and stem cell memory CD4+ T cells is associated with lack of progression in viremic individuals // PLoS Pathog. 2014. Vol. 10. P. e1004345.

Klatzmann D. et al. Selective tropism of lymphadenopathy associated virus (LAV) for helper-inducer T lymphocytes // Science. 1984. Vol. 225. P. 59‒63.

Li Q. et al. Simian immunodeficiency virus-induced intestinal cell apoptosis is the underlying mechanism of the regenerative enteropathy of early infection // J. Infect. Dis. 2008. Vol. 197. P. 420‒429.

Luciano A.A. et al. Impaired induction of CD27 and CD28 predicts naive CD4 T cell proliferation defects in HIV disease // J. Immunol. 2007. Vol. 179. P. 3543‒3549.

Mattapallil J.J. et al. Massive infection and loss of memory CD4+ T cells in multiple tissues during acute SIV infection // Nature. 2005. Vol. 434. P. 1093‒1097.

Moro-Garcia M.A., Alonso-Arias R., Lopez-Larrea C. When Aging Reaches CD4+ T-Cells: Phenotypic and Functional Changes // Front Immunol. 2013. Vol. 4. P. 107.

Okoye A. et al. Progressive CD4+ central memory T cell decline results in CD4+ effector memory insufficiency and overt disease in chronic SIV infection // J. Exp. Med. 2007. Vol. 204. P. 2171‒2185.

Okoye A.A., Picker L.J. CD4(+) T-cell depletion in HIV infection: mechanisms of immunological failure // Immunol. Rev. 2013. Vol. 254. P. 54‒64.

Okoye A.A. et al. Naive T cells are dispensable for memory CD4+ T cell homeostasis in progressive simian immunodeficiency virus infection // J. Exp. Med. 2012. Vol. 209. P. 641‒651.

Oliveira G. et al. Tracking genetically engineered lymphocytes long-term reveals the dynamics of T cell immunological memory // Sci. Transl. Med. 2015. Vol. 7. P. 317ra198.

Pacheco Y.M. et al. Risk factors, CD4 long-term evolution and mortality of HIV-infected patients who persistently maintain low CD4 counts, despite virological response to HAART // Curr. HIV Res. 2009. Vol. 7. P. 612‒619.

Pan X. et al. Restrictions to HIV-1 replication in resting CD4+ T lymphocytes // Cell Res. 2013. Vol. 23. P. 876‒885.

Pastor L. et al. Dynamics of CD4 and CD8 T-Cell Subsets and Inflammatory Biomarkers during Early and Chronic HIV Infection in Mozambican Adults // Front Immunol. 2017. Vol. 8. P. 1925.

Rallon N. et al. Central memory CD4 T cells are associated with incomplete restoration of the CD4 T cell pool after treatment-induced long-term undetectable HIV viraemia // J. Antimicrob. Chemother. 2013. Vol. 68. P. 2616‒2625.

Rethi B. et al. Loss of IL-7Ralpha is associated with CD4 T-cell depletion, high interleukin-7 levels and CD28 down-regulation in HIV infected patients // AIDS. 2005. Vol. 19. P. 2077‒2086.

Ribeiro R.M. et al. Naive and memory cell turnover as drivers of CCR5-to-CXCR4 tropism switch in human immunodeficiency virus type 1: implications for therapy // J. Virol. 2006. Vol. 80. P. 802‒809.

Ribeiro S.P. et al. The CD8(+) memory stem T cell (T(SCM)) subset is associated with improved prognosis in chronic HIV-1 infection // J. Virol. 2014. Vol. 88. P. 13836‒13844.

Roederer M. et al. CD8 naive T cell counts decrease progressively in HIV-infected adults // J. Clin. Invest. 1995. Vol. 95. P. 2061‒2066.

Safai B., Good R.A. Kaposi's sarcoma: a review and recent developments // CA Cancer. J. Clin. 1981. Vol. 31. P. 2‒12.

Sakaguchi S. et al. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases // J. Immunol. 1995. Vol. 155. P. 1151‒1164.

Sallusto F. et al. Two subsets of memory T lymphocytes with distinct homing potentials and effector functions // Nature. 1999. Vol. 401. P. 708‒712.

Schacker T.W. et al. Measurement of naive CD4 cells reliably predicts potential for immune reconstitution in HIV // J. Acquir. Immune Defic. Syndr. 2010. Vol. 54. P. 59‒62.

Schacker T.W. et al. Collagen deposition in HIV-1 infected lymphatic tissues and T cell homeostasis // Journal of Clinical Investigation. 2002. Vol. 110. P. 1133‒1139.

Schaerli P. et al. CXC chemokine receptor 5 expression defines follicular homing T cells with B cell helper function // J. Exp. Med. 2000. Vol. 192. P. 1553‒1562.

Schieferdecker H.L. et al. T cell differentiation antigens on lymphocytes in the human intestinal lamina propria // J. Immunol. 1992. Vol. 149. P. 2816‒2822.

Schnittman S.M. et al. Preferential infection of CD4+ memory T cells by human immunodeficiency virus type 1: evidence for a role in the selective T-cell functional defects observed in infected individuals // Proc. Natl. Acad. Sci. USA. 1990. Vol. 87. P. 6058‒6062.

Shmagel K.V et al. Influence of hepatitis C virus coinfection on CD4(+) T cells of HIV-infected patients receiving HAART // AIDS. 2014. Vol. 28. P. 2381‒2388.

Stevenson M. HIV-1 pathogenesis // Nat. Med. 2003. Vol. 9. P. 853‒860.

Trifari S. et al. Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from T(H)-17, T(H)1 and T(H)2 cells // Nat. Immunol. 2009. Vol. 10. P. 864‒871.

Veazey R.S. et al. Characterization of gut-associated lymphoid tissue (GALT) of normal rhesus macaques // Clin. Immunol. Immunopathol. 1997. Vol. 82. P. 230‒242.

Veldhoen M. et al. Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset // Nat. Immunol. 2008. Vol. 9. P. 1341‒1346.

Venzke S., Keppler O.T. Role of macrophages in HIV infection and persistence // Expert Rev. Clin. Immunol. 2006. Vol. 2. P. 613‒626.

Vrisekoop N. et al. Restoration of the CD4 T cell compartment after long-term highly active antiretroviral therapy without phenotypical signs of accelerated immunological aging // J. Immunol. 2008. Vol. 181. P. 1573‒1581.

Walzer P.D. et al. Pneumocystis carinii pneumonia in the United States. Epidemiologic, diagnostic, and clinical features // Ann. Intern. Med. 1974. Vol. 80. P. 83‒93.

Wang X., Mosmann T. In vivo priming of CD4 T cells that produce interleukin (IL)-2 but not IL-4 or interferon (IFN)-gamma, and can subsequently differentiate into IL-4- or IFN-gamma-secreting cells // J. Exp. Med. 2001. Vol. 194. P. 1069‒1080.

Zamarchi R. et al. Expression and functional activity of CXCR-4 and CCR-5 chemokine receptors in human thymocytes // Clin. Exp. Immunol. 2002. Vol. 127. P. 321‒330.

Zeng M., Haase A.T., Schacker T.W. Lymphoid tissue structure and HIV-1 infection: life or death for T cells // Trends Immunol. 2012. Vol. 33. P. 306‒314.

Zhou L., Chong M.M., Littman D.R., Plasticity of CD4+ T cell lineage differentiation // Immunity. 2009. Vol. 30. P. 646‒655.

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