Стрельцова Мария Алексеевна


Младший научный сотрудник (Лаборатория клеточных взаимодействий)

Тел.: +7 (495) 3304011

Эл. почта: mstreltsova@mail.ru

Образование

Период обученияСтрана, городУчебное заведениеДополнительная информация
2007–2012 Россия МГУ им. М.В.Ломоносова красный диплом

Членство в научных обществах

2011: член Российского биохимического общества

Гранты и проекты

ПериодДополнительная информация
2009–2013 «Анализ иммуномодулирующих эффектов миелопептидов, ганглиозидов, белков теплового шока и разработка подходов к их комбинированному применению для иммунотерапии»
2011–2014 «Сборная нано-система для активного контроля рака в продвинутой стадии: базовые наносистемы, доставка и попадание в опухоль, молекулярная визуализация, терапия на основе деградомного анализа»
2012–2014 «Наноконструкции для иммунотерапии рака на основе белков теплового шока»
2013–2014 "Разработка новых подходов к иммунодиагностике и иммунотерапии социально значимых заболеваний на основе эндогенных иммуномодуляторов и неприродных антител"
2014–2015 Грант РФФИ №14-04-32342 "Роль стресс-индуцируемых молекул MICA/B в вызываемых этанолом изменениях в функционировании иммунной системы". Руководитель.
2014–2016 Грант РФФИ №14-04-01842 "Разработка подходов к получению долгоживущих популяций NK-клеток человека с заданными характеристиками." Исполнитель

Избранные публикации

  1. Streltsova M.A., Barsov E., Erokhina S.A., Kovalenko E.I. (2017). Retroviral gene transfer into primary human NK cells activated by IL-2 and K562 feeder cells expressing membrane-bound IL-21. J. Immunol. Methods 450, 90–94 [+]

    Natural killer (NK) cells are capable of rapidly recognizing and efficiently killing tumor cells. This makes them a potentially promising agent for cancer immunotherapy. Additional genetic modifications of NK cells may further improve their anti-tumor efficacy. Numerous technical challenges associated with gene delivery into NK cells have significantly tempered this approach. We achieved efficient retroviral vector transduction of primary human NK cells that were stimulated by a combination of IL-2 and engineered K562 cells expressing membrane-bound IL-21. The activated NK cells were in less differentiated state and expressed NK cell activation receptors NKG2D, NKp30, CD16, and were highly HLA-DR-positive. This NK cell population was highly susceptible to the transduction by both GFP- and NGFR-expressing retroviral vectors, with transduction efficiency exceeding 50%. More mature CD57(+) NK cell population was generally resistant to retroviral vector transduction because of poor response to the stimulation. Our findings may facilitate retroviral vector-mediated genetic engineering of human primary NK cells for future immunotherapies.

    ID:1938
  2. Streltsova M.A., Klinkova A.V., Kuchukova A.A., Kadin A.Y., Kanevskiy L.M., Kovalenko E.I. (2016). Ethanol-dependent expression of the NKG2D ligands MICA/B in human cell lines and leukocytes. Biochem. Cell Biol. , 1–9 [+]

    Alcohol consumption affects the human immune system, causing a variety of disorders. However, the mechanisms of development of these changes are not fully understood. We hypothesized that ethanol may influence the expression of MICA and MICB, stress-induced molecules capable of regulating the activity of cytotoxic lymphocytes through the interaction with receptor NKG2D, which substantially affects the functionality of cellular immunity. We analyzed the effects of ethanol on MICA/B expression in tumor cell lines and human leukocytes. In the cell line models, ethanol caused different changes in the surface expression of MICA/B; in particular, it induced the translocation of intracellular proteins MICA/B to the cell surface and shedding of MICA (in soluble and microparticle-associated forms) from the plasma membrane. The observed results are not linked with cell death in cultures, taking place only under higher doses of ethanol. Ethanol at physiologically relevant concentrations (and higher) stimulated expression of MICA/B genes in different cell types. The effect of ethanol was more pronounced in hepatocyte line HepG2 compared with hematopoietic cell lines K562, Jurkat, and THP-1. Among the tested leukocytes, the most sensitive to ethanol action were T cells activated ex vivo with IL-2, in which the increase of MICA/B mRNA expression was registered with the smallest dose of ethanol (0.125%). In human monocytes, ethanol may lead to elevations in surface MICA/B levels. Presumably, changes in MICA/B expression caused by ethanol can affect the functions of NKG2D-positive cytotoxic lymphocytes, modulating immune reactions at excessive alcohol consumption.

    ID:1784
  3. Kanevskiy L.M., Erokhina S.A., Streltsova M.A., Telford W.G., Sapozhnikov A.M., Kovalenko E.I. (2014). Bacterial lipopolysaccharide activates CD57-negative human NK cells. Biochemistry Mosc. 79 (12), 1339–48 [+]

    NK cells play an important regulatory role in sepsis by induction and augmentation of proinflammatory reactions in early stages of the septic process and by suppression of immune response in later stages of inflammation. The present work was aimed at the effect of bacterial lipopolysaccharide (LPS), the main pathogenic factor of sepsis development, on human NK cells ex vivo. We show that LPS activates immature CD57-negative NK cells, which typically constitute less than half of the normal NK cell population in human peripheral blood. Under conditions of NK cell stimulation with IL-2, addition of LPS provokes an increase in IFN-γ production. However, LPS both increased and inhibited NK cell cytotoxic activity. It is important to note that the activation of NK cells on LPS addition was observed in the absence of TLR4 on the NK cell surface. These results confirm our previous data arguing for a direct interaction of LPS with NK cells and evidence an atypical mechanism of LPS-induced NK cell activation without the involvement of surface TLR4.

    ID:1258
  4. Kovalenko E., Kanevskiy L., Klinkova A., Kuchukova A., Streltsova M., Telford W., Sapozhnikov A. (2012). Stress-Induced Molecules in Regulation of NK Cell Activity. Chapter in a book “Cell Interaction” , 93–120 ID:1168