综述

实验性血管炎动物模型研究进展

展开
  • 上海交通大学医学院附属瑞金医院肾内科,上海 200025

收稿日期: 2020-09-09

  网络出版日期: 2022-07-26

基金资助

国家自然科学基金项目(81470041);国家自然科学基金项目(81000285)

本文引用格式

魏兆楠, 陈永熙 . 实验性血管炎动物模型研究进展[J]. 内科理论与实践, 2021 , 16(01) : 53 -59 . DOI: 10.16138/j.1673-6087.2021.01.012

参考文献

[1] Kitching AR, Anders HJ, Basu N, et al. ANCA-associated vasculitis[J]. Nat Rev Dis Primers, 2020, 6(1): 71.
[2] Kronbichler A, Shin JI, Lee KH, et al. Clinical associations of renal involvement in ANCA-associated vasculitis[J]. Autoimmun Rev, 2020, 19(4):102495.
[3] Centenera MM, Scott JS, Machiels J, et al. ELOVL5 is a critical and targetable fatty acid elongase in prostate cancer[J]. Cancer Res, 2021. [Epub ahead of print].
[4] 陈楠, 陈永熙. ANCA相关性小血管炎的肾外表现[J]. 临床肾脏病杂志, 2008, 28(5): 203-205.
[5] 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.
[6] Chen YX, Chen N. Pathogenesis of rapidly progressive glomerulonephritis: what do we learn[J]?. Contrib Nephrol, 2013, 181: 207-215.
[7] Chen YX, Chen XN. Antineutrophil cytoplasmic antibodies-associated glomerulonephritis: From bench to bedside[J]. Chronic Dis Transl Med, 2018, 4(3): 187-191.
[8] Chen YX, Xu J, Pan XX, et al. Histopathological classification and renal outcome in patients with antineutrophil cytoplasmic antibodies-associated renal vasculitis: a study of 186 patients and metaanalysis[J]. J Rheumatol, 2017, 44(3): 304-313.
[9] Chen YX, Yu HJ, Ni LY, et al. Propylthiouracil-associated antineutrophil cytoplasmic autoantibody-positive vasculitis: retrospective study of 19 cases[J]. J Rheumatol, 2007, 34(12): 2451-2456.
[10] Chen YX, Zhang W, Chen XN, et al. Propylthiouracil-induced antineutrophil cytoplasmic antibody (ANCA)-associated renal vasculitis versus primary ANCA-associated renal vasculitis: a comparative study[J]. J Rheumatol, 2012, 39(3): 558-563.
[11] Ramponi G, Folci M, De Santis M, et al. The biology, pathogenetic role, clinical implications, and open issues of serum anti-neutrophil cytoplasmic antibodies[J]. Autoimmun Rev, 2021. [Epub ahead of print].
[12] Nakazawa D, Masuda S, Tomaru U, et al. Pathogenesis and therapeutic interventions for ANCA-associated vasculitis[J]. Nat Rev Rheumatol, 2019, 15(2): 91-101.
[13] Esnault VL, Mathieson PW, Thiru S, et al. Autoantibodies to myeloperoxidase in brown Norway rats treated with mercuric chloride[J]. Lab Invest, 1992, 67(1): 114-120.
[14] Kinjoh K, Kyogoku M, Good RA. Genetic selection for crescent formation yields mouse strain with rapidly progressive glomerulonephritis and small vessel vasculitis[J]. Proc Natl Acad Sci U S A, 1993, 90(8): 3413-3417.
[15] Kobayashi K, Shibata T, Sugisaki T. Aggravation of rat nephrotoxic serum nephritis by anti-myeloperoxidase antibodies[J]. Kidney Int, 1995, 47(2): 454-463.
[16] Heeringa P, Brouwer E, Klok PA, et al. Autoantibodies to myeloperoxidase aggravate mild anti-glomerular-basement-membrane-mediated glomerular injury in the rat[J]. Am J Pathol, 1996, 149(5): 1695-1706.
[17] Brouwer E, Huitema MG, Klok PA, et al. Antimyeloperoxidase-associated proliferative glomerulonephritis: an animal model[J]. J Exp Med, 1993, 177(4): 905-914.
[18] Hutton HL, Holdsworth SR, Kitching AR. ANCA-associated vasculitis: pathogenesis, models, and preclinical testing[J]. Semin Nephrol, 2017, 37(5):418-435.
[19] Little MA, Smyth CL, Yadav R, et al. Antineutrophil cytoplasm antibodies directed against myeloperoxidase augment leukocyte-microvascular interactions in vivo[J]. Blood, 2005, 106(6): 2050-2058.
[20] Ruth AJ, Kitching AR, Kwan RY, et al. Anti-neutrophil cytoplasmic antibodies and effector CD4+ cells play nonredundant roles in anti-myeloperoxidase crescentic glomerulonephritis[J]. J Am Soc Nephrol, 2006, 17(7):1940-1949.
[21] Chang J, Eggenhuizen P, O’sullivan KM, et al. CD8+ T cells effect glomerular injury in experimental anti-myeloperoxidase GN[J]. J Am Soc Nephrol, 2017, 28(1): 47-55.
[22] Gan PY, O’sullivan KM, Ooi JD, et al. Mast cell stabilization ameliorates autoimmune anti-myeloperoxidase glomerulonephritis[J]. J Am Soc Nephrol, 2016, 27(5): 1321-1233.
[23] Odobasic D, Oudin V, Ito K, et al. Tolerogenic dendritic cells attenuate experimental autoimmune antimyeloperoxidase glomerulonephritis[J]. J Am Soc Nephrol, 2019, 30(11): 2140-2157.
[24] Gan PY, Chan A, Ooi JD, et al. Biologicals targeting T helper cell subset differentiating cytokines are effective in the treatment of murine anti-myeloperoxidase glomerulonephritis[J]. Kidney Int, 2019, 96(5): 1121-1133.
[25] Ooi JD, Jiang JH, Eggenhuizen PJ, et al. A plasmid-encoded peptide from Staphylococcus aureus induces anti-myeloperoxidase nephritogenic autoimmunity[J]. Nat Commun, 2019, 10(1): 3392.
[26] Ooi JD, Gan PY, Chen T, et al. FcγRIIB regulates T-cell autoreactivity, ANCA production, and neutrophil activation to suppress anti-myeloperoxidase glomerulonephritis[J]. Kidney Int, 2014, 86(6): 1140-1149.
[27] Xiao H, Heeringa P, Hu P, et al. Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice[J]. J Clin Invest, 2002, 110(7): 955-963.
[28] 安晓宁, 陈永熙. 单核-巨噬细胞在抗中性粒细胞胞浆抗体相关性血管炎中作用的研究进展[J]. 上海交通大学学报(医学版), 2020, 40(1): 123-127.
[29] Rousselle A, Kettritz R, Schreiber A. Monocytes promote crescent formation in anti-myeloperoxidase antibody-induced glomerulonephritis[J]. Am J Pathol, 2017, 187(9): 1908-1915.
[30] Hu P, Su H, Xiao H, et al. Kinin B1 receptor is important in the pathogenesis of myeloperoxidase-specific ANCA GN[J]. J Am Soc Nephrol, 2020, 31(2):297-307.
[31] Choi M, Schreiber A, Eulenberg-Gustavus C, et al. Endothelial NF-κB blockade abrogates ANCA-induced GN[J]. J Am Soc Nephrol, 2017, 28(11): 3191-3204.
[32] Wang Q, van Timmeren MM, Petersen AH, et al. Age-determined severity of anti-myeloperoxidase autoantibody-mediated glomerulonephritis in mice[J]. Nephrol Dial Transplant, 2017, 32(2): 254-264.
[33] Xiao H, Ciavatta D, Aylor DL, et al. Genetically determined severity of anti-myeloperoxidase glomerulonephritis[J]. Am J Pathol, 2013, 182(4): 1219-1226.
[34] Schreiber A, Xiao H, Falk RJ, et al. Bone marrow-derived cells are sufficient and necessary targets to mediate glomerulonephritis and vasculitis induced by anti-myeloperoxidase antibodies[J]. J Am Soc Nephrol, 2006, 17(12): 3355-3364.
[35] Ooi JD, Chang J, Hickey MJ, et al. The immunodominant myeloperoxidase T-cell epitope induces local cell-mediated injury in antimyeloperoxidase glomerulonephritis[J]. Proc Natl Acad Sci U S A, 2012, 109(39): E2615-E2624.
[36] Gan PY, Holdsworth SR, Kitching AR, et al. Myeloperoxidase (MPO)-specific CD4+ T cells contribute to MPO-anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis[J]. Cell Immunol, 2013, 282(1): 21-27.
[37] Pfister H, Ollert M, Fröhlich LF, et al. Antineutrophil cytoplasmic autoantibodies against the murine homolog of proteinase 3 (Wegener autoantigen) are pathogenic in vivo[J]. Blood, 2004, 104(5): 1411-1418.
[38] van Der Geld YM, Hellmark T, Selga D, et al. Rats and mice immunised with chimeric human/mouse proteinase 3 produce autoantibodies to mouse Pr3 and rat granulocytes[J]. Ann Rheum Dis, 2007, 66(12): 1679-1682.
[39] Primo VC, Marusic S, Franklin CC, et al. Anti-PR3 immune responses induce segmental and necrotizing glomerulonephritis[J]. Clin Exp Immunol, 2010, 159(3): 327-337.
[40] Little MA, Al-Ani B, Ren S, et al. Anti-proteinase 3 anti-neutrophil cytoplasm autoantibodies recapitulate systemic vasculitis in mice with a humanized immune system[J]. PLoS One, 2012, 7(1): e28626.
[41] Li N, Zhu B, Zhu Q, et al. Serum lysosomal-associated membrane protein-2 levels are increased in small and medium-vessel vasculitis, especially in polyarteritis nodosa[J]. Clin Exp Rheumatol, 2019, 37 Suppl 117(2):79-85.
[42] Tang S, Zhang Y, Yin SW, et al. Neutrophil extracellular trap formation is associated with autophagy-related signalling in ANCA-associated vasculitis[J]. Clin Exp Immunol, 2015, 180(3): 408-418.
[43] Sangaletti S, Tripodo C, Chiodoni C, et al. Neutrophil extracellular traps mediate transfer of cytoplasmic neutrophil antigens to myeloid dendritic cells toward ANCA induction and associated autoimmunity[J]. Blood, 2012, 120(15): 3007-3018.
[44] Nakazawa D, Tomaru U, Suzuki A, et al. Abnormal conformation and impaired degradation of propylthiouracil-induced neutrophil extracellular traps: implications of disordered neutrophil extracellular traps in a rat model of myeloperoxidase antineutrophil cytoplasmic antibody-associated vasculitis[J]. Arthritis Rheum, 2012, 64(11): 3779-3787.
[45] Martin KR, Pederzoli-Ribeil M, Pacreau E, et al. Transgenic mice expressing human proteinase 3 exhibit sustained neutrophil-associated peritonitis[J]. J Immunol, 2017, 199(11): 3914-3924.
[46] Merkel PA, Xie G, Monach PA, et al. Identification of functional and expression polymorphisms associated with risk for antineutrophil cytoplasmic autoantibody-associated vasculitis[J]. Arthritis Rheumatol, 2017, 69(5):1054-1066.
[47] Nusser A, Nuber N, Wirz OF, et al. The development of autoimmune features in aging mice is closely associated with alterations of the peripheral CD4+ T-cell compartment[J]. Eur J Immunol, 2014, 44(10): 2893-2902.
[48] Tao L, Reese TA. Making mouse models that reflect human immune responses[J]. Trends Immunol, 2017, 38(3):181-193.
文章导航

/