The role of complement in autoimmune renal disease

被引:27
作者
Seelen, M. A.
Daha, M. R.
机构
[1] Univ Groningen, Dept Internal Med, Renal Transplantat Unit, Med Ctr, NL-9700 RB Groningen, Netherlands
[2] Leiden Univ, Ctr Med, Dept Nephrol, Leiden, Netherlands
关键词
autoimmune diseases; complement activation; autoantibodies; subepithelial immune complex;
D O I
10.1080/08916930600739688
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The predominance of renal involvement in autoimmune diseases can most likely be assigned to the specialised function of the kidneys filtrating over 120 ml plasma per minute. Complement activation by autoantibodies directed against planted antigens or antigens already present in renal tissue in the subendothelial and mesangial regions provoke an inflammatory response ultimately resulting in renal damage. New data also suggest complement involvement in the pathogenesis of renal disease caused by subepithelial immune complex deposition. On the other hand complement itself can also be a target of an autoimmune responses causing renal damage as seen in SLE. The results on intervention of complement activation in clinical practise are awaited.
引用
收藏
页码:411 / 415
页数:5
相关论文
共 34 条
  • [1] Membranoproliferative glomerulonephritis type II (dense deposit disease):: An update
    Appel, GB
    Cook, HT
    Hageman, G
    Jennette, JC
    Kashgarian, M
    Kirschfink, M
    Lambris, JD
    Lanning, L
    Lutz, HU
    Meri, S
    Rose, NR
    Salant, DJ
    Sethi, S
    Smith, RJH
    Smoyer, W
    Tully, HF
    Tully, SP
    Walker, P
    Welsh, M
    Würzner, R
    Zipfel, PF
    [J]. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2005, 16 (05): : 1392 - 1403
  • [2] Development of autoantibodies before the clinical onset of systemic lupus erythematosus
    Arbuckle, MR
    McClain, MT
    Rubertone, MV
    Scofield, RH
    Dennis, GJ
    James, JA
    Harley, JB
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (16) : 1526 - 1533
  • [3] Therapeutic inhibition of the complement system. Y2K update
    Asghar, SS
    Pasch, MC
    [J]. FRONTIERS IN BIOSCIENCE-LANDMARK, 2000, 5 : E63 - E82A
  • [4] C5a promotes development of experimental lupus nephritis which can be blocked with a specific receptor antagonist
    Bao, LH
    Osawe, I
    Puri, T
    Lambris, JD
    Haas, M
    Quigg, RJ
    [J]. EUROPEAN JOURNAL OF IMMUNOLOGY, 2005, 35 (08) : 2496 - 2506
  • [5] Administration of a soluble recombinant complement C3 inhibitor protects against renal disease in MRL/lpr mice
    Bao, LH
    Haas, M
    Kraus, DM
    Hack, BK
    Rakstang, JK
    Holers, VM
    Quigg, RJ
    [J]. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2003, 14 (03): : 670 - 679
  • [6] Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies
    Botto, M
    Dell'Agnola, C
    Bygrave, AE
    Thompson, EM
    Cook, HT
    Petry, F
    Loos, M
    Pandolfi, PP
    Walport, MJ
    [J]. NATURE GENETICS, 1998, 19 (01) : 56 - 59
  • [7] C1q, autoimmunity and apoptosis
    Botto, M
    Walport, MJ
    [J]. IMMUNOBIOLOGY, 2002, 205 (4-5) : 395 - 406
  • [8] AUTOANTIGENS TARGETED IN SYSTEMIC LUPUS-ERYTHEMATOSUS ARE CLUSTERED IN 2 POPULATIONS OF SURFACE-STRUCTURES ON APOPTOTIC KERATINOCYTES
    CASCIOLAROSEN, LA
    ANHALT, G
    ROSEN, A
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (04) : 1317 - 1330
  • [9] COUSER WG, 1995, J AM SOC NEPHROL, V5, P1888
  • [10] Contrasting roles of complement activation and its regulation in membranous nephropathy
    Cunningham, PN
    Quigg, RJ
    [J]. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2005, 16 (05): : 1214 - 1222