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感染与中性粒细胞胞质抗体相关性血管炎间相关性的研究进展

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  • 上海交通大学医学院附属瑞金医院肾脏科,上海 200025

收稿日期: 2018-07-04

  网络出版日期: 2019-12-25

本文引用格式

徐婷婷, 张文 . 感染与中性粒细胞胞质抗体相关性血管炎间相关性的研究进展[J]. 诊断学理论与实践, 2019 , 18(06) : 698 -703 . DOI: 10.16150/j.1671-2870.2019.06.019

参考文献

[1] Watts RA, Mahr A, Mohammad AJ, et al. Classification, epidemiology and clinical subgrouping of antineutrophil cytoplasmic antibody(ANCA)-associated vasculitis[J]. Nephrol Dial Transplant, 2015, 30(Suppl 1):i14-i22.
[2] Chen YX, Yu HJ, Zhang W, et al. Analyzing fatal cases of Chinese patients with primary antineutrophil cytoplasmic antibodies-associated renal vasculitis: a 10-year retrospective study[J]. Kidney Blood Press Res. 2008; 31(5):343-349.
[3] Itabashi M, Takei T, Yabuki Y, et al. Clinical outcome and prognosis of anti-neutrophil cytoplasmic antibody-associated vasculitis in Japan[J]. Nephron Clin Pract, 2010, 115(1):c21-c27.
[4] Guillevin L, Cordier JF, Lhote F, et al. A prospective, multicenter, randomized trial comparing steroids and pulse cyclophosphamide versus steroids and oral cyclophosphamide in the treatment of generalized Wege-ner's granulomatosis[J]. Arthritis Rheum, 1997, 40(12):2187-2198.
[5] Kronbichler A, Jayne DR, Mayer G. Frequency, risk factors and prophylaxis of infection in ANCA-associated vasculitis[J]. Eur J Clin Invest, 2015, 45(3):346-368.
[6] Sada KE, Yamamura M, Harigai M, et al. Different responses to treatment across classified diseases and severities in Japanese patients with microscopic polyangiitis and granulomatosis with polyangiitis: a nationwide prospective inception cohort study[J]. Arthritis Res Ther, 2015, 17:305.
[7] Goupil R, Brachemi S, Nadeau-Fredette AC, et al. Lymphopenia and treatment-related infectious complications in ANCA-associated vasculitis[J]. Clin J Am Soc Nephrol, 2013, 8(3):416-423.
[8] Harper L, Savage CO. ANCA-associated renal vasculitis at the end of the twentieth century--a disease of older patients[J]. Rheumatology (Oxford), 2005, 44(4):495-501.
[9] Guerry MJ, Brogan P, Bruce IN, et al. Recommendations for the use of rituximab in anti-neutrophil cytoplasm antibody-associated vasculitis[J]. Rheumatology (Oxford), 2012, 51(4):634-643.
[10] Charlier C, Henegar C, Launay O, et al. Risk factors for major infections in Wegener granulomatosis: analysis of 113 patients[J]. Ann Rheum Dis, 2009, 68(5):658-663.
[11] Charles P, Néel A, Tieulié N, et al. Rituximab for induction and maintenance treatment of ANCA-associated vasculitides: a multicentre retrospective study on 80 patients[J]. Rheumatology (Oxford), 2014, 53(3):532-539.
[12] Yates M, Watts RA, Bajema IM, et al. EULAR/ERA-EDTA recommendations for the management of ANCA-associated vasculitis[J]. Ann Rheum Dis, 2016, 75(9):1583-1594.
[13] Kronbichler A, Kerschbaum J, Gopaluni S, et al. Trimethoprim-sulfamethoxazole prophylaxis prevents severe/life-threatening infections following rituximab in antineutrophil cytoplasm antibody-associated vasculitis[J]. Ann Rheum Dis, 2018, 77(10):1440-1447.
[14] Cartin-Ceba R, Golbin JM, Keogh KA, et al. Rituximab for remission induction and maintenance in refractory granulomatosis with polyangiitis(Wegener's): ten-year experience at a single center[J]. Arthritis Rheum, 2012, 64(11):3770-3778.
[15] Pendergraft WF 3rd, Preston GA, Shah RR, et al. Autoimmunity is triggered by cPR-3(105-201), a protein complementary to human autoantigen proteinase-3[J]. Nat Med, 2004, 10(1):72-79.
[16] Kain R, Exner M, Brandes R, et al. Molecular mimicry in pauci-immune focal necrotizing glomerulonephritis[J]. Nat Med, 2008, 14(10):1088-1096.
[17] Roth AJ, Brown MC, Smith RN, et al. Anti-LAMP-2 antibodies are not prevalent in patients with antineutrophil cytoplasmic autoantibody glomerulonephritis[J]. J Am Soc Nephrol, 2012, 23(3):545-555.
[18] Peschel A, Basu N, Benharkou A, et al. Autoantibodies to hLAMP-2 in ANCA-negative pauci-immune focal necrotizing GN[J]. J Am Soc Nephrol, 2014, 25(3):455-463.
[19] Takeuchi S, Kimura S, Soma Y, et al. Lysosomal-associa-ted membrane protein-2 plays an important role in the pathogenesis of primary cutaneous vasculitis[J]. Rheumatology (Oxford), 2013, 52(9):1592-1598.
[20] Zielinski CE, Mele F, Aschenbrenner D, et al. Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β[J]. Nature, 2012, 484(7395):514-518.
[21] Dong X, Bachman LA, Miller MN, et al. Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction[J]. Kidney Int, 2008, 74(10):1294-1309.
[22] Paust HJ, Turner JE, Steinmetz OM, et al. The IL-23/Th17 axis contributes to renal injury in experimental glomerulonephritis[J]. J Am Soc Nephrol, 2009, 20(5):969-979.
[23] Wilde B, Thewissen M, Damoiseaux J, et al. Th17 expansion in granulomatosis with polyangiitis (Wegener's): the role of disease activity, immune regulation and therapy[J]. Arthritis Res Ther, 2012, 14(5):R227.
[24] Free ME, Bunch DO, McGregor JA, et al. Patients with antineutrophil cytoplasmic antibody-associated vasculitis have defective Treg cell function exacerbated by the presence of a suppression-resistant effector cell population[J]. Arthritis Rheum, 2013, 65(7):1922-1933.
[25] Velden J, Paust HJ, Hoxha E, et al. Renal IL-17 expression in human ANCA-associated glomerulonephritis[J]. Am J Physiol Renal Physiol, 2012, 302(12):F1663-F1673.
[26] Krebs CF, Paust HJ, Krohn S, et al. Autoimmune renal disease is exacerbated by S1P-receptor-1-dependent intestinal Th17 cell migration to the kidney[J]. Immunity, 2016, 45(5):1078-1092.
[27] Savage CO, Gaskin G, Pusey CD, et al. Myeloperoxidase binds to vascular endothelial cells, is recognized by ANCA and can enhance complement dependent cytotoxicity[J]. Adv Exp Med Biol, 1993, 336:121-123.
[28] Jennette JC, Falk RJ. Pathogenesis of antineutrophil cytoplasmic autoantibody-mediated disease[J]. Nat Rev Rheumatol, 2014, 10(8):463-473.
[29] Huang YM, Wang H, Wang C, et al. Promotion of hypercoagulability in antineutrophil cytoplasmic antibody-associated vasculitis by C5a-induced tissue factor-expressing microparticles and neutrophil extracellular traps[J]. Arthritis Rheumatol, 2015, 67(10):2780-2790.
[30] Kantari C, Pederzoli-Ribeil M, Amir-Moazami O, et al. Proteinase 3, the Wegener autoantigen, is externalized during neutrophil apoptosis: evidence for a functional association with phospholipid scramblase 1 and interfere-nce with macrophage phagocytosis[J]. Blood, 2007, 110(12):4086-4095.
[31] Millet A, Martin KR, Bonnefoy F, et al. Proteinase 3 on apoptotic cells disrupts immune silencing in autoimmune vasculitis[J]. J Clin Invest, 2015, 125(11):4107-4121.
[32] Kanehisa M, Goto S, Sato Y, et al. KEGG for integration and interpretation of large-scale molecular data sets[J]. Nucleic Acids Res, 2012,40(Database issue):D109-D114.
[33] Kerstein A, Schüler S, Cabral-Marques O, et al. Environmental factor and inflammation-driven alteration of the total peripheral T-cell compartment in granulomatosis with polyangiitis[J]. J Autoimmun, 2017, 78:79-91.
[34] Laudien M, Gadola SD, Podschun R, et al. Nasal carriage of Staphylococcus aureus and endonasal activity in Wegener s granulomatosis as compared to rheumatoid arthritis and chronic Rhinosinusitis with nasal polyps[J]. Clin Exp Rheumatol, 2010, 28(1 Suppl 57):51-55.
[35] Addy C, Doran G, Jones AL, et al. Microscopic polyangii-tis secondary to Mycobacterium abscessus in a patient with bronchiectasis: a case report[J]. BMC Pulm Med, 2018, 18(1):170.
[36] Iijima Y, Kobayashi Y, Uchida Y, et al. A case report of granulomatous polyangiitis complicated by tuberculous lymphadenitis[J]. Medicine (Baltimore), 2018, 97(43):e12430.
[37] Fukusumi M, Miyazaki K, Shibata M, et al. A case of Wegener granulomatosis after treatment for non-tuberculous mycobacteriosis[J]. Nihon Kokyuki Gakkai Zasshi, 2011, 49(1):37-43.
[38] Yamaguchi M, Yoshioka T, Yamakawa T, et al. Anti-neutrophil cytoplasmic antibody-associated vasculitis associated with infectious mononucleosis due to primary Epstein-Barr virus infection: report of three cases[J]. Clin Kidney J, 2014, 7(1):45-48.
[39] Meyer MF, Hellmich B, Kotterba S, et al. Cytomegalovirus infection in systemic necrotizing vasculitis: causative agent or opportunistic infection?[J]. Rheumatol Int, 2000, 20(1):35-38.
[40] Lidar M, Lipschitz N, Langevitz P, et al. Infectious serologies and autoantibodies in Wegener's granulomatosis and other vasculitides: novel associations disclosed using the Rad BioPlex 2200[J]. Ann N Y Acad Sci, 2009, 1173:649-657.
[41] Marshak-Rothstein A. Toll-like receptors in systemic autoimmune disease[J]. Nat Rev Immunol, 2006, 6(11):823-835.
[42] Uezono S, Sato Y, Hara S, et al. Outcome of ANCA-associated primary renal vasculitis in Miyazaki Prefecture[J]. Intern Med, 2007, 46(12):815-822.
[43] Matsumoto Y, Sada KE, Otsuka F, et al. Evaluation of weekly-reduction regimen of glucocorticoids in combination with cyclophosphamide for anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis in Japanese patients[J]. Rheumatol Int, 2012, 32(10):2999-3005.
[44] Godeau B, Mainardi JL, Roudot-Thoraval F, et al. Factors associated with Pneumocystis carinii pneumonia in Wegener's granulomatosis[J]. Ann Rheum Dis, 1995, 54(12):991-994.
[45] Weidanz F, Day CJ, Hewins P, et al. Recurrences and infections during continuous immunosuppressive therapy after beginning dialysis in ANCA-associated vasculitis[J]. Am J Kidney Dis, 2007, 50(1):36-46.
[46] Lionaki S, Hogan SL, Jennette CE, et al. The clinical course of ANCA small-vessel vasculitis on chronic dialysis[J]. Kidney Int, 2009, 76(6):644-651.
[47] Flossmann O, Berden A, de Groot K, et al. Long-term patient survival in ANCA-associated vasculitis[J]. Ann Rheum Dis, 2011, 70(3):488-494.
[48] Bligny D, Mahr A, Toumelin PL, et al. Predicting mortality in systemic Wegener's granulomatosis: a survival analysis based on 93 patients[J]. Arthritis Rheum, 2004, 51(1):83-91.
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