DNaseI in pathogenesis of systemic lupus erythematosus

被引：39

作者：

Tsukumo, SI ^{[1
]}

Yasutomo, K ^{[1
]}

机构：

[1] Univ Tokushima, Grad Sch, Inst Hlth Biosci, Dept Immunol & Parasitol, Tokushima 7708503, Japan

来源：

CLINICAL IMMUNOLOGY | 2004年 / 113卷 / 01期

关键词：

autoimmune diseases; systemic lupus erythematosus; DNaseI;

D O I：

10.1016/j.clim.2004.05.009

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 aberrant activation of lymphocytes causes autoimmune diseases. Although there are many candidate molecules that are involved in the pathogenesis of autoimmune diseases, it still remains unclear how immunological tolerance is disturbed in each autoimmune disease. Recently, we discovered two patients suffering from systemic lupus erythematosus (SLE) with a defect in the DNaseI gene locus. According to immunological and genetic analysis, we hypothesize that defective antigen clearance, especially accumulation of nucleosomal antigens, is responsible for the development of SLE. In this article, we review the pathogenesis of SLE from the view of defective self-antigen clearance due to low DNaseI activity. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：14 / 18

页数：5

共 42 条

[1] Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity [J].

Bickerstaff, MCM ;

Botto, M ;

Hutchinson, WL ;

Herbert, J ;

Tennent, GA ;

Bybee, A ;

Mitchell, DA ;

Cook, HT ;

Butler, PJG ;

Walport, MJ ;

Pepys, MB .

NATURE MEDICINE, 1999, 5 (06) :694-697

[2] Accelerated development of IgG autoantibodies and autoimmune disease in the absence of secreted IgM [J].

Boes, M ;

Schmidt, T ;

Linkemann, K ;

Beaudette, BC ;

Marshak-Rothstein, A ;

Chen, JZ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (03) :1184-1189

[3] Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies [J].

Botto, M ;

Dell'Agnola, C ;

Bygrave, AE ;

Thompson, EM ;

Cook, HT ;

Petry, F ;

Loos, M ;

Pandolfi, PP ;

Walport, MJ .

NATURE GENETICS, 1998, 19 (01) :56-59

[4]

BRENNAN FM, 1988, IMMUNOLOGY, V63, P213

[5] SERUM DEOXYRIBONUCLEASE-I AND CLINICAL ACTIVITY IN SYSTEMIC LUPUS-ERYTHEMATOSUS [J].

CHITRABAMRUNG, S ;

RUBIN, RL ;

TAN, EM .

RHEUMATOLOGY INTERNATIONAL, 1981, 1 (02) :55-60

[6] Advances in immunology - Autoimmune diseases [J].

Davidson, A ;

Diamond, B .

NEW ENGLAND JOURNAL OF MEDICINE, 2001, 345 (05) :340-350

[7] Recombinant human Dnase I (rhDNase) in patients with lupus nephritis [J].

Davis, JC ;

Manzi, S ;

Yarboro, C ;

Rairie, J ;

Mcinnes, I ;

Averthelyi, D ;

Sinicropi, D ;

Hale, VG ;

Balow, J ;

Austin, H ;

Boumpas, DT ;

Klippel, JH .

LUPUS, 1999, 8 (01) :68-76

[8] CORRELATION BETWEEN LEVELS OF DNA ANTIBODIES AND CLINICAL DISEASE ACTIVITY IN SLE - RETROSPECTIVE EVALUATION [J].

DAVIS, P ;

PERCY, JS ;

RUSSELL, AS .

ANNALS OF THE RHEUMATIC DISEASES, 1977, 36 (02) :157-159

[9] A subset of lupus anti-DNA antibodies cross-reacts with the NR2 glutamate receptor in systemic lupus erythematosus [J].

DeGiorgio, LA ;

Konstantinov, KN ;

Lee, SC ;

Hardin, JA ;

Volpe, BT ;

Diamond, B .

NATURE MEDICINE, 2001, 7 (11) :1189-1193

[10] Antigenic triggers and molecular targets for anti-double-stranded DNA antibodies [J].

Deocharan, B ;

Qing, X ;

Beger, E ;

Putterman, C .

LUPUS, 2002, 11 (12) :865-871

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