Systemic lupus-erythematosus:: Deoxyribonuclease 1 in necrotic chromatin disposal

被引:41
作者
Napirei, M
Gültekin, A
Kloeckl, T
Möröy, T
Frostegård, J
Mannherz, HG
机构
[1] Ruhr Univ Bochum, Fak Med, Abt Anat & Embryol, D-4630 Bochum, Germany
[2] Univ Klinikum, IFZ, Inst Zellbiol Tumorforsch, Essen, Germany
[3] Karolinska Hosp, Dept Rheumatol, S-10401 Stockholm, Sweden
关键词
deoxyribonuclease; 1; systemic lupus-erythematosus; DNA-degradation; necrosis;
D O I
10.1016/j.biocel.2005.10.023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Systemic lupus-erythematosus is an auto-immune-disease characterized by pathogenic anti-nuclear auto-antibodies. These form immune-complexes that after deposition at basal membranes at various locations initiate inflammatory reactions. There is a clear genetic and gender predisposition (females are affected 10 times more frequently), but also infectious agents and further environmental factors have been shown to be causative for the initiation of the disease. It has been suggested that the auto-antibodies arise after release and/or inefficient removal of nuclear components during cell death (defective cellular "waste disposal" theory). So far, increased apoptotic cell death has been made responsible, but recent data suggest that defective cellular waste disposal during/after necrosis may also lead to the release and prolonged exposure of nuclear components. Here, we concentrate on chromatin disposal during necrosis and the involvement of Deoxyribonuclease I in this process with respect to its possible role in the prevention of anti-nuclear auto-immunity. (C) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:297 / 306
页数:10
相关论文
共 44 条
[1]  
[Anonymous], DUBOIS LUPUS ERYTHEM
[2]   Antigen presentation by macrophages is enhanced by the uptake of necrotic, but not apoptotic, cells [J].
Barker, RN ;
Erwig, LP ;
Hill, KSK ;
Devine, A ;
Pearce, WP ;
Rees, AJ .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2002, 127 (02) :220-225
[3]  
BASNAKIAN AG, 2005, J AM SOC NEHROL
[4]   Spontaneous autoimmunity in 129 and C57BL/6 mice - Implications for autoimmunity described in gene-targeted mice [J].
Bygrave, AE ;
Rose, KL ;
Cortes-Hernandez, J ;
Warren, J ;
Rigby, RJ ;
Cook, HT ;
Walport, MJ ;
Vyse, TJ ;
Botto, M .
PLOS BIOLOGY, 2004, 2 (08) :1081-1090
[5]   The A/T mutation in exon 2 of the DNASE1 gene is not present in Tunisian patients with systemic lupus erythematosus or in healthy subjects [J].
Chakraborty, P ;
Kacem, HH ;
Makni-Karray, K ;
Jarraya, F ;
Ayadi, H .
ARTHRITIS AND RHEUMATISM, 2003, 48 (11) :3297-3298
[6]   SERUM DEOXYRIBONUCLEASE-I AND CLINICAL ACTIVITY IN SYSTEMIC LUPUS-ERYTHEMATOSUS [J].
CHITRABAMRUNG, S ;
RUBIN, RL ;
TAN, EM .
RHEUMATOLOGY INTERNATIONAL, 1981, 1 (02) :55-60
[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]  
Dong Z, 1997, AM J PATHOL, V151, P1205
[9]   DEATH AND THE CELL [J].
DUVALL, E ;
WYLLIE, AH .
IMMUNOLOGY TODAY, 1986, 7 (04) :115-119
[10]   Defects in the disposal of dying cells lead to autoimmunity. [J].
Gaipl U.S. ;
Franz S. ;
Voll R.E. ;
Sheriff A. ;
Kalden J.R. ;
Herrmann M. .
Current Rheumatology Reports, 2004, 6 (6) :401-407