Нарушение баланса провоспалительных цитокинов и Т-регуляторных клеток у больных хроническим гломерулонефритом
Нарушение баланса провоспалительных цитокинов и Т-регуляторных клеток у больных хроническим гломерулонефритом
Чеботарева Н.В., Виноградов А.А., Гиндис А.А. и др. Нарушение баланса провоспалительных цитокинов и Т-регуляторных клеток у больных хроническим гломерулонефритом. Терапевтический архив. 2020; 92 (6): 46–52.
DOI: 10.26442/00403660.2020.06.000671
DOI: 10.26442/00403660.2020.06.000671
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Аннотация
Хронический гломерулонефрит (ХГН) является заболеванием с неуклонно прогрессирующим течением, в основе которого лежит воспаление с активацией иммунных клеток. Выраженность воспалительной реакции в ткани почки определяется балансом локально воздействующих провоспалительных факторов и защитных механизмов, к которым относят продукцию Т-регуляторными (Т-рег) лимфоцитами противовоспалительных цитокинов. Изучение процессов, способных модулировать выраженность воспаления в почке, приобретает особый интерес для понимания основных закономерностей прогрессирования ХГН.
Цель. Определить клиническое значение цитокинов Th17, Th1 и Тreg в моче для оценки активности и прогрессирования ХГН с нефротическим синдромом (НС).
Материалы и методы. В исследование включены 98 больных ХГН – 37 женщин и 61 мужчина. В зависимости от степени активности ХГН пациенты разделены на 2 группы. 1-я состояла из 51 пациента с НС. У 21 исследуемого выявлено снижение скорости клубочковой фильтрации ниже 60 мл/мин. Во 2-й группе – 47 пациентов с протеинурией от 1 до 3 г/сут без НС. У 26 больных наблюдалось снижение скорости клубочковой фильтрации ниже 60 мл/мин/1,73 м2. Проведена биопсия почки и верифицирован морфологический диагноз 65 пациентам: у 20 – мезангиопролиферативный гломерулонефрит, 16 – мембранозная нефропатия, 18 – фокально-сегментарный гломерулосклероз (ФСГС), 11 – мембранопролиферативный гломерулонефрит. Группа контроля состояла из 15 здоровых людей. Уровни интерлейкинов – ИЛ-6, ИЛ-10, ИЛ-17, фактора некроза опухоли a (ФНО-a) в моче определяли с помощью иммуноферментного анализа. У 39 пациентов в биоптате выявили количество FoxP3-положительных клеток в воспалительном интерстициальном инфильтрате коркового слоя на участке 1,5 мм2.
Результаты. В общей группе больных ХГН отмечалось повышение уровня цитокинов Th17, Th1 и Treg в моче: ФНО-a и ИЛ-10 по сравнению со здоровыми лицами. Повышение уровня ИЛ-6 в моче больных с высокой клинической активностью ХГН (с НС и дисфункцией почек) более выражено, чем у пациентов с НС и сохранной функцией почек. У больных ХГН с НС по сравнению с пациентами без НС отмечены уменьшение количества T-рег клеток в интерстиции почки и снижение продукции противовоспалительного ИЛ-10. Наиболее значимые изменения цитокинового профиля с повышением провоспалительных цитокинов и снижением Т-рег в ткани почки и противовоспалительного ИЛ-10 в моче зафиксированы у больных ФСГС с НС.
Заключение. У больных ХГН с НС, особенно при ФСГС, отмечается дисбаланс цитокинов, характеризующийся повышенным уровнем в моче провоспалительных ИЛ-17, ИЛ-6, ФНО-a, сниженным уровнем противовоспалительного ИЛ-10 и Т-рег лимфоцитов в ткани почки. Нарушение баланса цитокинов отражает высокую активность ХГН и риск его прогрессирования.
Ключевые слова: интерлейкин-17, интерлейкин-6, интерлейкин-10, фактор некроза опухоли αa, Т-регуляторные клетки, хронический гломерулонефрит.
Aim. To determine the clinical significance of the Th17, Th1, and Treg cytokines in urine to assess the activity and progression of chronic glomerulonephritis with nephrotic syndrome (NS).
Materials and methods. The study included 98 patients with CGN – 37 women and 61 men. Patients were divided into two groups according to the degree of CGN activity. Group I consisted of 51 patients with NS. In 21 subjects, a decrease in GFR<60 ml/min was revealed. Group II included 47 patients with proteinuria from 1 to 3 g/day without NS. GFR<60 ml/min/1.73 m2 was observed in
26 patients. A kidney biopsy was performed in 65 patients and the hystological diagnosis was verified: 20 had mesangioproliferative GN, 16 had membranous nephropathy, 18 had focal segmental glomerulosclerosis, and 11 had membranoproliferative GN. The control group consisted of 15 healthy people. The levels of IL-6, IL-10, IL-17, tumor necrosis factor a (TNF-a) in the urine were determined using enzyme-linked immunosorbent assay. The number of FoxP3-positive cells in the inflammatory interstitial infiltrate of the cortical layer was determined in 39 patients (in a biopsy sample in a 1.5 mm2 area).
Results. In group of patients with CGN, there was an increase in the levels of Th17, Th1, and Treg cytokines in urine – TNF-a and IL-10 compared with healthy individuals. An increase in the levels of IL-6 in the urine of patients with high clinical activity of CGN (with NS and renal dysfunction) was more pronounced than in patients with NS and normal renal function. There was a decrease in the number of Treg cells in the interstitium of the kidney and a decrease in the production of anti-inflammatory IL-10 in CGN patients with NS, compared with patients without NS. The most pronounced changes in the cytokine profile were observed in patients with FSGS with an increase in pro-inflammatory cytokines and a decrease in Treg in the kidney tissue/anti-inflammatory IL-10 in the urine.
Conclusion. An imbalance of cytokines characterized by an increased levels of pro-inflammatory IL-17, IL-6, TNF-a, and a reduced levels of anti-inflammatory IL-10 and T-regulatory cells in the kidney tissue is noted in patients with NS, especially with FSGS. Imbalance of cytokines reflects the high activity of CGN and the risk of the progression of the disease.
Keywords: interleukin-17, interleukin-6, interleukin-10, tumor necrosis factor αa, Treg cells, chronic glomerulonephritis.
Цель. Определить клиническое значение цитокинов Th17, Th1 и Тreg в моче для оценки активности и прогрессирования ХГН с нефротическим синдромом (НС).
Материалы и методы. В исследование включены 98 больных ХГН – 37 женщин и 61 мужчина. В зависимости от степени активности ХГН пациенты разделены на 2 группы. 1-я состояла из 51 пациента с НС. У 21 исследуемого выявлено снижение скорости клубочковой фильтрации ниже 60 мл/мин. Во 2-й группе – 47 пациентов с протеинурией от 1 до 3 г/сут без НС. У 26 больных наблюдалось снижение скорости клубочковой фильтрации ниже 60 мл/мин/1,73 м2. Проведена биопсия почки и верифицирован морфологический диагноз 65 пациентам: у 20 – мезангиопролиферативный гломерулонефрит, 16 – мембранозная нефропатия, 18 – фокально-сегментарный гломерулосклероз (ФСГС), 11 – мембранопролиферативный гломерулонефрит. Группа контроля состояла из 15 здоровых людей. Уровни интерлейкинов – ИЛ-6, ИЛ-10, ИЛ-17, фактора некроза опухоли a (ФНО-a) в моче определяли с помощью иммуноферментного анализа. У 39 пациентов в биоптате выявили количество FoxP3-положительных клеток в воспалительном интерстициальном инфильтрате коркового слоя на участке 1,5 мм2.
Результаты. В общей группе больных ХГН отмечалось повышение уровня цитокинов Th17, Th1 и Treg в моче: ФНО-a и ИЛ-10 по сравнению со здоровыми лицами. Повышение уровня ИЛ-6 в моче больных с высокой клинической активностью ХГН (с НС и дисфункцией почек) более выражено, чем у пациентов с НС и сохранной функцией почек. У больных ХГН с НС по сравнению с пациентами без НС отмечены уменьшение количества T-рег клеток в интерстиции почки и снижение продукции противовоспалительного ИЛ-10. Наиболее значимые изменения цитокинового профиля с повышением провоспалительных цитокинов и снижением Т-рег в ткани почки и противовоспалительного ИЛ-10 в моче зафиксированы у больных ФСГС с НС.
Заключение. У больных ХГН с НС, особенно при ФСГС, отмечается дисбаланс цитокинов, характеризующийся повышенным уровнем в моче провоспалительных ИЛ-17, ИЛ-6, ФНО-a, сниженным уровнем противовоспалительного ИЛ-10 и Т-рег лимфоцитов в ткани почки. Нарушение баланса цитокинов отражает высокую активность ХГН и риск его прогрессирования.
Ключевые слова: интерлейкин-17, интерлейкин-6, интерлейкин-10, фактор некроза опухоли αa, Т-регуляторные клетки, хронический гломерулонефрит.
________________________________________________
Aim. To determine the clinical significance of the Th17, Th1, and Treg cytokines in urine to assess the activity and progression of chronic glomerulonephritis with nephrotic syndrome (NS).
Materials and methods. The study included 98 patients with CGN – 37 women and 61 men. Patients were divided into two groups according to the degree of CGN activity. Group I consisted of 51 patients with NS. In 21 subjects, a decrease in GFR<60 ml/min was revealed. Group II included 47 patients with proteinuria from 1 to 3 g/day without NS. GFR<60 ml/min/1.73 m2 was observed in
26 patients. A kidney biopsy was performed in 65 patients and the hystological diagnosis was verified: 20 had mesangioproliferative GN, 16 had membranous nephropathy, 18 had focal segmental glomerulosclerosis, and 11 had membranoproliferative GN. The control group consisted of 15 healthy people. The levels of IL-6, IL-10, IL-17, tumor necrosis factor a (TNF-a) in the urine were determined using enzyme-linked immunosorbent assay. The number of FoxP3-positive cells in the inflammatory interstitial infiltrate of the cortical layer was determined in 39 patients (in a biopsy sample in a 1.5 mm2 area).
Results. In group of patients with CGN, there was an increase in the levels of Th17, Th1, and Treg cytokines in urine – TNF-a and IL-10 compared with healthy individuals. An increase in the levels of IL-6 in the urine of patients with high clinical activity of CGN (with NS and renal dysfunction) was more pronounced than in patients with NS and normal renal function. There was a decrease in the number of Treg cells in the interstitium of the kidney and a decrease in the production of anti-inflammatory IL-10 in CGN patients with NS, compared with patients without NS. The most pronounced changes in the cytokine profile were observed in patients with FSGS with an increase in pro-inflammatory cytokines and a decrease in Treg in the kidney tissue/anti-inflammatory IL-10 in the urine.
Conclusion. An imbalance of cytokines characterized by an increased levels of pro-inflammatory IL-17, IL-6, TNF-a, and a reduced levels of anti-inflammatory IL-10 and T-regulatory cells in the kidney tissue is noted in patients with NS, especially with FSGS. Imbalance of cytokines reflects the high activity of CGN and the risk of the progression of the disease.
Keywords: interleukin-17, interleukin-6, interleukin-10, tumor necrosis factor αa, Treg cells, chronic glomerulonephritis.
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54. McCarthy ET, Sharma R, Sharma M, et al. TNF-alpha increases albumin permeability of isolated rat glomeruli through the generation of superoxide. J Am Soc Nephrol. 1998;9(3):433-8.
55. Pedigo CE, Ducasa GM, Leclercq F, et al. Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injury. J Clin Invest. 2016;126(9):3336-50. doi: 10.1172/jci85939
56. Bakr A, Shokeir M, El-Chenawi F, et al. Tumor necrosis factor-α production from mononuclear cells in nephrotic syndrome. Pediatr Nephrol. 2003;18(6):516-20. doi: 10.1007/s00467-003-1122-4
57. Bitzan M, Babayeva S, Vasudevan A, et al. TNFα pathway blockade ameliorates toxic effects of FSGS plasma on podocyte cytoskeleton and β3 integrin activation. Pediatr Nephrol. 2012;27(12):2217-26. doi: 10.1007/s00467-012-2163-3
58. Leroy S, Guigonis V, Bruckner D, et al. Successful Anti‐TNFα Treatment in a Child with Posttransplant Recurrent Focal Segmental Glomerulosclerosis. Am J Transplant. 2009;9(4):858-61. doi: 10.1111/j.1600-6143.2009.02550.x
2. Stangou M, Bantis C, Skoularopoulou M, et al. Th1, Th2 and Treg/T17 cytokines in two types of proliferative glomerulonephritis. Indian J Nephrol. 2016;26(3):159. doi: 10.4103/0971-4065.159303
3. Turner JE, Paust HJ, Steinmetz OM, Panzer U. The Th17 immune response in renal inflammation. Kidney Int. 2010;77(12): 1070-5. doi: 10.1038/ki.2010.102
4. Mosmann TR, Coffman RL. TH1 and TH2 Cells: Different Patterns of Lymphokine Secretion Lead to Different Functional Properties. Annu Rev Immunol. 1989;7(1):145-73. doi: 10.1146/annurev.iy.07.040189.001045
5. Harrington LE, Hatton RD, Mangan PR, 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;6(11):1123-32. doi: 10.1038/ni1254
6. Lai Kwan Lam Q, King Hung Ko O, Zheng BJ, Lu L. Local BAFF gene silencing suppresses Th17-cell generation and ameliorates autoimmune arthritis. Proc Natl Acad Sci USA. 2008;105(39):14993-8. doi: 10.1073/pnas.0806044105
7. Maloy KJ. The Interleukin-23/Interleukin-17 axis in intestinal inflammation. J Intern Med. 2008;263(6):584-90. doi: 10.1111/j.1365-2796.2008.01950.x
8. Molet S, Hamid Q, Davoineb F, et al. IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines. J Allergy Clin Immunol. 2001;108(3):430-8. doi: 10.1067/mai.2001.117929
9. Chen DY, Chen YM, Wen MC, et al. The potential role of Th17 cells and Th17-related cytokines in the pathogenesis of lupus nephritis. Lupus. 2012;21(13):1385-96. doi: 10.1177/0961203312457718
10. Mansouri M, Mansouri P, Raze AA, Jadali Z. The potential role of Th17 lymphocytes in patients with psoriasis. An Bras Dermatol. 2018;93(1):63-6. doi: 10.1590/abd1806-4841.20186123
11. McGeachy MJ, Cua DJ. Th17 Cell Differentiation: The Long and Winding Road. Immunity. 2008;28(4):445-53. doi: 10.1016/j.immuni.2008.03.001
12. Rodrigues-Díez R, Rodrigues-Díez RR, Rayego-Mateos S, et al. The C-terminal module IV of connective tissue growth factor is a novel immune modulator of the Th17 response. Lab Invest. 2013;93(7):812-24. doi: 10.1038/labinvest.2013.67
13. Zhu S, Qian Y. IL-17/IL-17 receptor system in autoimmune disease: mechanisms and therapeutic potential. Clin Sci. 2012;122(11):487-511. doi: 10.1042/cs20110496
14. Kolls JK, Lindén A. Interleukin-17 Family Members and Inflammation. Immunity. 2004;21(4);467-76. doi: 10.1016/j.immuni.2004.08.018
15. Ley K, Smith E, Stark MA. IL-17A-producing neutrophil-regulatory Tn lymphocytes. Immunol Res. 2006;34(3):229-42. doi: 10.1385/ir:34:3:229
16. Stark MA, Huo Y, Burcin TL, et al. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17. Immunity. 2005;22(3):285-94. doi: 10.1016/j.immuni.2005.01.011
17. Niemir ZI, Ondracek M, Dworacki G, et al. In situ upregulation of IL-10 reflects the activity of human glomerulonephritides. Am J Kidney Dis. 1998;32(1):80-92. doi: 10.1053/ajkd.1998.v32.pm9669428
18. Ouyang W, Rutz S, Crellin NK, et al. Regulation and functions of the
IL-10 family of cytokines in inflammation and disease. Annu Rev Immunol. 2011;29(1):71-109. doi: 10.1146/annurev-immunol-031210-101312
19. Zhang R, Li Q, Chuang PY, et al. Regulation of pathogenic Th17 cell differentiation by IL-10 in the development of glomerulonephritis. Am J Pathol. 2013;183(2):402-12. doi: 10.1016/j.ajpath.2013.05.001
20. Kalavrizioti D, Gerolymos M, Rodi M, et al. T helper (Th)-cytokines in the urine of patients with primary glomerulonephritis treated with immunosuppressive drugs: Can they predict outcome? Cytokine. 2015;76(2):260-9. doi: 10.1016/j.cyto.2015.08.002
21. Wang L, Li Q, Wang L, et al. The role of Th17/IL-17 in the pathogenesis of primary nephrotic syndrome in children. Kidney Blood Press Res. 2013;37(1):332-45. doi: 10.1159/000350161
22. Korn T, Bettelli E, Oukka M, Kuchroo VK. IL-17 and Th17 Cells. Ann Rev Immunol. 2009;27(1)6:485-517. doi: 10.1146/annurev.immunol.
021908.132710
23. Ogura H, Murakami M, Okuyama Y, et al. Interleukin-17 promotes autoimmunity by triggering a positive-feedback loop via interleukin-6 induction. Immunity. 2008;29(4):628-36. doi: 10.1016/j.immuni.2008.07.018
24. Matsumoto K, Kanmatsuse К. Increased Urinary Excretion of Interleukin-17 in Nephrotic Patients. Nephron. 2002;91(1):243-9. doi: 10.1159/000058399
25. Velden J, Paust HJ, Hoxha E, et al. Renal IL-17 expression in human ANCA-associated glomerulonephritis. Am J Physiol Renal Physiol. 2012;302(1):1663-73. doi: 10.1152/ajprenal.00683.2011
26. Strehlau J, de Haij S, Boonstra JG, et al. Quantitative detection of immune activation transcripts as a diagnostic tool in kidney transplantation. Proc Natl Acad Sci USA. 1997;94(2):695-700. doi: 10.1073/pnas.94.2.695
27. Kawaguchi M, Kokubu F, Kuga H, et al. Modulation of bronchial epithelial cells by IL-17. J Allergy Clin Immunol. 2001;108(5):804-9. doi: 10.1067/mai.2001.119027
28. Von Vietinghoff S, Ley K. Homeostatic regulation of blood neutrophil counts. J Immunol. 2008;181(8):5183-8. doi: 10.4049/jimmunol.181.8.5183
29. O’Quinn D, Palmer M, Lee Y, Weaver C. Emergence of the Th17 pathway and its role in host defense. Adv Immunol. 2008;99(1):115-63. doi: 10.1016/s0065-2776(08)00605-6
30. Mangan PR, Harrington LE, O’Quinn DB, et al. Transforming growth factor-beta induces development of the TH17 lineage. Nature. 2006;441(7090):231-4. doi: 10.1038/nature04754
31. Veldhoen M, Hocking RJ, Atkins CJ, et al. TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity. 2006;24(2):179-89. doi: 10.1016/j.immuni.2006.01.001
32. Liu HP, Cao AT, Feng T, et al. TGF-β converts Th1 cells into Th17 cells through stimulation of Runx1 expression. Eur J Immunol. 2015;45(4):1010-8. doi: 10.1002/eji.201444726
33. Zhang J, Li Y, Shan K, et al. Sublytic C5b-9 induces IL-6 and TGF-beta1 production by glomerular mesangial cells in rat Thy-1 nephritis through p300-mediated C/EBPbeta acetylation. FASEB J. 2014;28(3):1511-25. doi: 10.1096/fj.13-242693
34. Zhang W, Wang W, Yu H, et al. Interleukin 6 underlies angiotensin II- induced hypertension and chronic renal damage. Hypertension. 2012;59(1):136-44. doi: 10.1161/hypertensionaha.111.173328
35. Zhang XL, Topley N, Ito T, Phillips A. Interleukin-6 regulation of transforming growth factor (TGF)-beta receptor compartmentalization and turnover enhances TGF-beta1 signaling. J Biol Chem. 2005;280(13):12239-45. doi: 10.1074/jbc.m413284200
36. Paun A, Bergeron ME, Haston CK. The Th1/Th17 balance dictates the fibrosis response in murine radiation-induced lung disease. Sci Reports. 2017;7(1). doi: 10.1038/s41598-017-11656-5
37. Lei L, Zhao C, Qin F, et al. Th17 cells and IL-17 promote the skin and lung inflammation and fibrosis process in a bleomycin-induced murine model of systemic sclerosis. Clin Exp Rheumatol. 2016;34 Suppl. 100(5):14-22. PMID: 26750756.
38. Shao XS, Yang XQ, Zhao XD, et al. The prevalence of Th17 cells and FOXP3 regulate T cells (Treg) in children with primary nephritic syndrome. Pediatr Nephrol. 2009;24(9):1683-90. doi: 10.1007/s00467-009-1194-x
39. Liu LL, Qin Y, Cai JF, et al. Th17/Treg imbalance in adult patients with minimal change nephrotic syndrome. Clin Immunol. 2011;139(3):314-20. doi: 10.1016/j.clim.2011.02.018
40. Homey B. After TH1⁄TH2 now comes Treg⁄TH17: significance of T helper cells in immune response organization. Hautarzt. 2006;57(8):730-2. doi: 10.1007/s00105-006-1199-3
41. Sakaguchi S, Ono M, Setoguchi R, et al. Foxp3+CD25+CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease. Immunol Rev. 2006;212(1):8-27. doi: 10.1111/j.0105-2896.2006.00427.x
42. Wolf D, Hochegger K, Wolf AM, et al. CD4+/CD25+ regulatory T cells inhibit experimental anti-glomerular basement membrane glomerulonephritis in mice. J Am Soc Nephrol. 2005;16(5):1360-70. doi: 10.1681/asn.2004100837
43. Miossec P, Kolls JK. Targeting IL-17 and TH17 cells in chronic inflammation. Nat Rev Drug Discov. 2012;11(10):763-76. doi: 10.1038/nrd3794
44. Strassmann G, Patil-Koota V, Finkelman F, et al. Evidence for the involvement of interleukin 10 in the differential deactivation of murine peritoneal macrophages by prostaglandin E2. J Exp Med. 1994;180(6):2365-70. doi: 10.1084/jem.180.6.2365
45. Lewkowicz P, Lewkowicz N, Sasiak A, Tchorzewski H. Lipopolysaccharide-activated CD4+/CD25+ T regulatory T cells inhibit neutrophil function and promote their apoptosis and death. J Immunol. 2006;177(10):7155-63. doi: 10.4049/jimmunol.177.10.7155
46. Mertz PM, de Witt DL, Stetler-Stevenson WG, Wahl LM. Interleukin 10 supression of monocyte prostaglandin H synthase-2. Mechanism of inhibition of prostaglandin-dependent matrix metalloproteinase production. J Biol Chem. 1994;269:21322-9.
47. Olszina DP, Pajkrt D, Lauw FN, van Deventer SJ. Interleukin-10 inhibits the release of CC chemokines during human endotoxemia. J Infect Dis. 2000;181(2):613-20. doi: 10.1086/315275
48. Taams LS, van Amelsfort JM, Tiemessen MM, et al. Modulation of monocyte/macrophage function by human CD4+/CD25+ regulatory T cells. Hum Immunol. 2005;66(3):222-30. doi: 10.1016/j.humimm.2004.12.006
49. Mistra N, Bayry J, Lacroix-Desmazes S, et al. Cutting edge: human CD4+/CD25+ T cells restrain the maturation and antigen-presenting function of dendritic cells. J Immunol. 2004;172(8):4676-80. doi: 10.4049/jimmunol.172.8.4676
50. Lim HW, Hillsamer P, Banham AH, Kim CH. Cutting edge: direct suppression of B cells by CD4+/CD25+ regulatory T cells. J Immunol. 2005;175(7):4180-3. doi: 10.4049/jimmunol.175.7.4180
51. Shalhoub RJ. Pathogenesis of lipoid nephrosis: a disorder of T-cell function. Lancet. 1974;304(7880):556-60. doi: 10.1016/s0140-6736(74)91880-7
52. Savin VJ, Sharma R, Sharma M, et al. Circulating factor associated with increased glomerular permeability to albumin in recurrent focal segmental glomerulosclerosis. N Engl J Med. 1996;334(14):878-83. doi: 10.1056/nejm199604043341402
53. Suranyi MG, Guasch A, Hall BM, Myers BD. Elevated Levels of Tumor Necrosis Factor-α in the Nephrotic Syndrome in Humans. Am J Kidney Dis. 1993;21(3):251-9. doi: 10.1016/s0272-6386(12)80742-6
54. McCarthy ET, Sharma R, Sharma M, et al. TNF-alpha increases albumin permeability of isolated rat glomeruli through the generation of superoxide. J Am Soc Nephrol. 1998;9(3):433-8.
55. Pedigo CE, Ducasa GM, Leclercq F, et al. Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injury. J Clin Invest. 2016;126(9):3336-50. doi: 10.1172/jci85939
56. Bakr A, Shokeir M, El-Chenawi F, et al. Tumor necrosis factor-α production from mononuclear cells in nephrotic syndrome. Pediatr Nephrol. 2003;18(6):516-20. doi: 10.1007/s00467-003-1122-4
57. Bitzan M, Babayeva S, Vasudevan A, et al. TNFα pathway blockade ameliorates toxic effects of FSGS plasma on podocyte cytoskeleton and β3 integrin activation. Pediatr Nephrol. 2012;27(12):2217-26. doi: 10.1007/s00467-012-2163-3
58. Leroy S, Guigonis V, Bruckner D, et al. Successful Anti‐TNFα Treatment in a Child with Posttransplant Recurrent Focal Segmental Glomerulosclerosis. Am J Transplant. 2009;9(4):858-61. doi: 10.1111/j.1600-6143.2009.02550.x
2. Stangou M, Bantis C, Skoularopoulou M, et al. Th1, Th2 and Treg/T17 cytokines in two types of proliferative glomerulonephritis. Indian J Nephrol. 2016;26(3):159. doi: 10.4103/0971-4065.159303
3. Turner JE, Paust HJ, Steinmetz OM, Panzer U. The Th17 immune response in renal inflammation. Kidney Int. 2010;77(12): 1070-5. doi: 10.1038/ki.2010.102
4. Mosmann TR, Coffman RL. TH1 and TH2 Cells: Different Patterns of Lymphokine Secretion Lead to Different Functional Properties. Annu Rev Immunol. 1989;7(1):145-73. doi: 10.1146/annurev.iy.07.040189.001045
5. Harrington LE, Hatton RD, Mangan PR, 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;6(11):1123-32. doi: 10.1038/ni1254
6. Lai Kwan Lam Q, King Hung Ko O, Zheng BJ, Lu L. Local BAFF gene silencing suppresses Th17-cell generation and ameliorates autoimmune arthritis. Proc Natl Acad Sci USA. 2008;105(39):14993-8. doi: 10.1073/pnas.0806044105
7. Maloy KJ. The Interleukin-23/Interleukin-17 axis in intestinal inflammation. J Intern Med. 2008;263(6):584-90. doi: 10.1111/j.1365-2796.2008.01950.x
8. Molet S, Hamid Q, Davoineb F, et al. IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines. J Allergy Clin Immunol. 2001;108(3):430-8. doi: 10.1067/mai.2001.117929
9. Chen DY, Chen YM, Wen MC, et al. The potential role of Th17 cells and Th17-related cytokines in the pathogenesis of lupus nephritis. Lupus. 2012;21(13):1385-96. doi: 10.1177/0961203312457718
10. Mansouri M, Mansouri P, Raze AA, Jadali Z. The potential role of Th17 lymphocytes in patients with psoriasis. An Bras Dermatol. 2018;93(1):63-6. doi: 10.1590/abd1806-4841.20186123
11. McGeachy MJ, Cua DJ. Th17 Cell Differentiation: The Long and Winding Road. Immunity. 2008;28(4):445-53. doi: 10.1016/j.immuni.2008.03.001
12. Rodrigues-Díez R, Rodrigues-Díez RR, Rayego-Mateos S, et al. The C-terminal module IV of connective tissue growth factor is a novel immune modulator of the Th17 response. Lab Invest. 2013;93(7):812-24. doi: 10.1038/labinvest.2013.67
13. Zhu S, Qian Y. IL-17/IL-17 receptor system in autoimmune disease: mechanisms and therapeutic potential. Clin Sci. 2012;122(11):487-511. doi: 10.1042/cs20110496
14. Kolls JK, Lindén A. Interleukin-17 Family Members and Inflammation. Immunity. 2004;21(4);467-76. doi: 10.1016/j.immuni.2004.08.018
15. Ley K, Smith E, Stark MA. IL-17A-producing neutrophil-regulatory Tn lymphocytes. Immunol Res. 2006;34(3):229-42. doi: 10.1385/ir:34:3:229
16. Stark MA, Huo Y, Burcin TL, et al. Phagocytosis of apoptotic neutrophils regulates granulopoiesis via IL-23 and IL-17. Immunity. 2005;22(3):285-94. doi: 10.1016/j.immuni.2005.01.011
17. Niemir ZI, Ondracek M, Dworacki G, et al. In situ upregulation of IL-10 reflects the activity of human glomerulonephritides. Am J Kidney Dis. 1998;32(1):80-92. doi: 10.1053/ajkd.1998.v32.pm9669428
18. Ouyang W, Rutz S, Crellin NK, et al. Regulation and functions of the
IL-10 family of cytokines in inflammation and disease. Annu Rev Immunol. 2011;29(1):71-109. doi: 10.1146/annurev-immunol-031210-101312
19. Zhang R, Li Q, Chuang PY, et al. Regulation of pathogenic Th17 cell differentiation by IL-10 in the development of glomerulonephritis. Am J Pathol. 2013;183(2):402-12. doi: 10.1016/j.ajpath.2013.05.001
20. Kalavrizioti D, Gerolymos M, Rodi M, et al. T helper (Th)-cytokines in the urine of patients with primary glomerulonephritis treated with immunosuppressive drugs: Can they predict outcome? Cytokine. 2015;76(2):260-9. doi: 10.1016/j.cyto.2015.08.002
21. Wang L, Li Q, Wang L, et al. The role of Th17/IL-17 in the pathogenesis of primary nephrotic syndrome in children. Kidney Blood Press Res. 2013;37(1):332-45. doi: 10.1159/000350161
22. Korn T, Bettelli E, Oukka M, Kuchroo VK. IL-17 and Th17 Cells. Ann Rev Immunol. 2009;27(1)6:485-517. doi: 10.1146/annurev.immunol.
021908.132710
23. Ogura H, Murakami M, Okuyama Y, et al. Interleukin-17 promotes autoimmunity by triggering a positive-feedback loop via interleukin-6 induction. Immunity. 2008;29(4):628-36. doi: 10.1016/j.immuni.2008.07.018
24. Matsumoto K, Kanmatsuse К. Increased Urinary Excretion of Interleukin-17 in Nephrotic Patients. Nephron. 2002;91(1):243-9. doi: 10.1159/000058399
25. Velden J, Paust HJ, Hoxha E, et al. Renal IL-17 expression in human ANCA-associated glomerulonephritis. Am J Physiol Renal Physiol. 2012;302(1):1663-73. doi: 10.1152/ajprenal.00683.2011
26. Strehlau J, de Haij S, Boonstra JG, et al. Quantitative detection of immune activation transcripts as a diagnostic tool in kidney transplantation. Proc Natl Acad Sci USA. 1997;94(2):695-700. doi: 10.1073/pnas.94.2.695
27. Kawaguchi M, Kokubu F, Kuga H, et al. Modulation of bronchial epithelial cells by IL-17. J Allergy Clin Immunol. 2001;108(5):804-9. doi: 10.1067/mai.2001.119027
28. Von Vietinghoff S, Ley K. Homeostatic regulation of blood neutrophil counts. J Immunol. 2008;181(8):5183-8. doi: 10.4049/jimmunol.181.8.5183
29. O’Quinn D, Palmer M, Lee Y, Weaver C. Emergence of the Th17 pathway and its role in host defense. Adv Immunol. 2008;99(1):115-63. doi: 10.1016/s0065-2776(08)00605-6
30. Mangan PR, Harrington LE, O’Quinn DB, et al. Transforming growth factor-beta induces development of the TH17 lineage. Nature. 2006;441(7090):231-4. doi: 10.1038/nature04754
31. Veldhoen M, Hocking RJ, Atkins CJ, et al. TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity. 2006;24(2):179-89. doi: 10.1016/j.immuni.2006.01.001
32. Liu HP, Cao AT, Feng T, et al. TGF-β converts Th1 cells into Th17 cells through stimulation of Runx1 expression. Eur J Immunol. 2015;45(4):1010-8. doi: 10.1002/eji.201444726
33. Zhang J, Li Y, Shan K, et al. Sublytic C5b-9 induces IL-6 and TGF-beta1 production by glomerular mesangial cells in rat Thy-1 nephritis through p300-mediated C/EBPbeta acetylation. FASEB J. 2014;28(3):1511-25. doi: 10.1096/fj.13-242693
34. Zhang W, Wang W, Yu H, et al. Interleukin 6 underlies angiotensin II- induced hypertension and chronic renal damage. Hypertension. 2012;59(1):136-44. doi: 10.1161/hypertensionaha.111.173328
35. Zhang XL, Topley N, Ito T, Phillips A. Interleukin-6 regulation of transforming growth factor (TGF)-beta receptor compartmentalization and turnover enhances TGF-beta1 signaling. J Biol Chem. 2005;280(13):12239-45. doi: 10.1074/jbc.m413284200
36. Paun A, Bergeron ME, Haston CK. The Th1/Th17 balance dictates the fibrosis response in murine radiation-induced lung disease. Sci Reports. 2017;7(1). doi: 10.1038/s41598-017-11656-5
37. Lei L, Zhao C, Qin F, et al. Th17 cells and IL-17 promote the skin and lung inflammation and fibrosis process in a bleomycin-induced murine model of systemic sclerosis. Clin Exp Rheumatol. 2016;34 Suppl. 100(5):14-22. PMID: 26750756.
38. Shao XS, Yang XQ, Zhao XD, et al. The prevalence of Th17 cells and FOXP3 regulate T cells (Treg) in children with primary nephritic syndrome. Pediatr Nephrol. 2009;24(9):1683-90. doi: 10.1007/s00467-009-1194-x
39. Liu LL, Qin Y, Cai JF, et al. Th17/Treg imbalance in adult patients with minimal change nephrotic syndrome. Clin Immunol. 2011;139(3):314-20. doi: 10.1016/j.clim.2011.02.018
40. Homey B. After TH1⁄TH2 now comes Treg⁄TH17: significance of T helper cells in immune response organization. Hautarzt. 2006;57(8):730-2. doi: 10.1007/s00105-006-1199-3
41. Sakaguchi S, Ono M, Setoguchi R, et al. Foxp3+CD25+CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease. Immunol Rev. 2006;212(1):8-27. doi: 10.1111/j.0105-2896.2006.00427.x
42. Wolf D, Hochegger K, Wolf AM, et al. CD4+/CD25+ regulatory T cells inhibit experimental anti-glomerular basement membrane glomerulonephritis in mice. J Am Soc Nephrol. 2005;16(5):1360-70. doi: 10.1681/asn.2004100837
43. Miossec P, Kolls JK. Targeting IL-17 and TH17 cells in chronic inflammation. Nat Rev Drug Discov. 2012;11(10):763-76. doi: 10.1038/nrd3794
44. Strassmann G, Patil-Koota V, Finkelman F, et al. Evidence for the involvement of interleukin 10 in the differential deactivation of murine peritoneal macrophages by prostaglandin E2. J Exp Med. 1994;180(6):2365-70. doi: 10.1084/jem.180.6.2365
45. Lewkowicz P, Lewkowicz N, Sasiak A, Tchorzewski H. Lipopolysaccharide-activated CD4+/CD25+ T regulatory T cells inhibit neutrophil function and promote their apoptosis and death. J Immunol. 2006;177(10):7155-63. doi: 10.4049/jimmunol.177.10.7155
46. Mertz PM, de Witt DL, Stetler-Stevenson WG, Wahl LM. Interleukin 10 supression of monocyte prostaglandin H synthase-2. Mechanism of inhibition of prostaglandin-dependent matrix metalloproteinase production. J Biol Chem. 1994;269:21322-9.
47. Olszina DP, Pajkrt D, Lauw FN, van Deventer SJ. Interleukin-10 inhibits the release of CC chemokines during human endotoxemia. J Infect Dis. 2000;181(2):613-20. doi: 10.1086/315275
48. Taams LS, van Amelsfort JM, Tiemessen MM, et al. Modulation of monocyte/macrophage function by human CD4+/CD25+ regulatory T cells. Hum Immunol. 2005;66(3):222-30. doi: 10.1016/j.humimm.2004.12.006
49. Mistra N, Bayry J, Lacroix-Desmazes S, et al. Cutting edge: human CD4+/CD25+ T cells restrain the maturation and antigen-presenting function of dendritic cells. J Immunol. 2004;172(8):4676-80. doi: 10.4049/jimmunol.172.8.4676
50. Lim HW, Hillsamer P, Banham AH, Kim CH. Cutting edge: direct suppression of B cells by CD4+/CD25+ regulatory T cells. J Immunol. 2005;175(7):4180-3. doi: 10.4049/jimmunol.175.7.4180
51. Shalhoub RJ. Pathogenesis of lipoid nephrosis: a disorder of T-cell function. Lancet. 1974;304(7880):556-60. doi: 10.1016/s0140-6736(74)91880-7
52. Savin VJ, Sharma R, Sharma M, et al. Circulating factor associated with increased glomerular permeability to albumin in recurrent focal segmental glomerulosclerosis. N Engl J Med. 1996;334(14):878-83. doi: 10.1056/nejm199604043341402
53. Suranyi MG, Guasch A, Hall BM, Myers BD. Elevated Levels of Tumor Necrosis Factor-α in the Nephrotic Syndrome in Humans. Am J Kidney Dis. 1993;21(3):251-9. doi: 10.1016/s0272-6386(12)80742-6
54. McCarthy ET, Sharma R, Sharma M, et al. TNF-alpha increases albumin permeability of isolated rat glomeruli through the generation of superoxide. J Am Soc Nephrol. 1998;9(3):433-8.
55. Pedigo CE, Ducasa GM, Leclercq F, et al. Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injury. J Clin Invest. 2016;126(9):3336-50. doi: 10.1172/jci85939
56. Bakr A, Shokeir M, El-Chenawi F, et al. Tumor necrosis factor-α production from mononuclear cells in nephrotic syndrome. Pediatr Nephrol. 2003;18(6):516-20. doi: 10.1007/s00467-003-1122-4
57. Bitzan M, Babayeva S, Vasudevan A, et al. TNFα pathway blockade ameliorates toxic effects of FSGS plasma on podocyte cytoskeleton and β3 integrin activation. Pediatr Nephrol. 2012;27(12):2217-26. doi: 10.1007/s00467-012-2163-3
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Авторы
Н.В. Чеботарева1, А.А. Виноградов2, А.А. Гиндис1, И.Н. Бобкова1, В. Цао1, Л.В. Лысенко1
1 ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России
(Сеченовский Университет), Москва, Россия;
2 ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова», Москва, Россия
1 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia;
2 Lomonosov Moscow State University, Moscow, Russia
1 ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России
(Сеченовский Университет), Москва, Россия;
2 ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова», Москва, Россия
________________________________________________
1 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia;
2 Lomonosov Moscow State University, Moscow, Russia
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