Clearance deficiency-A potential link between infections and autoimmunity

被引：69

作者：

Schulze, C. ^{[1
]}

Munoz, L. E. ^{[1
]}

Franz, S. ^{[1
]}

Sarter, K. ^{[1
]}

Chaurio, R. A. ^{[1
]}

Gaipl, U. S. ^{[2
]}

Herrmann, M. ^{[1
]}

机构：

[1] Friedrich Alexander Univ Erlangen Nuremberg, Dept Internal Med 3, Inst Clin Immunol & Rheumatol, D-91054 Erlangen, Germany

[2] Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Dept Radiat Oncol, D-91054 Erlangen, Germany

来源：

AUTOIMMUNITY REVIEWS | 2008年 / 8卷 / 01期

关键词：

Apoptosis; Clearance deficiency; SLE; Inflammation;

D O I：

10.1016/j.autrev.2008.07.049

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Cell death plays a pivotal role in development and homeostasis of multicellular organisms. Apoptosis represents the physiological and anti-inflammatory form of cell death. Advanced apoptosis and necrosis are rather pro-inflammatory. Several "find-me"- and "eat-me"-signals support the "swift and silent" removal of dying cells. If the highly controlled process of dying cell removal fails, they may progress to secondary necrosis and provoke autoimmunity. There are several reports describing clearance deficiency as a possible mechanism in the etiopathogenesis of SLE. Under certain conditions, increased phagocytosis of nuclear material may be found in a subgroup of patients with SLE. Complement proteins and autoantibodies may modify engulfment of apoptotic remnants and shift the clearance process towards inflammation. Taken together, clearance deficiency leads to the accumulation of apoptotic remnants and breaking of tolerance to self Besides, enhanced uptake of nuclear immune complexes may maintain chronic autoimmunity in patients with SLE. (C) 2008 Elsevier BY. All rights reserved.

引用

页码：5 / 8

页数：4

共 34 条

[1]

Baumann I, 2002, ARTHRITIS RHEUM-US, V46, P191, DOI 10.1002/1529-0131(200201)46:1<191::AID-ART10027>3.0.CO

[2]

2-K

[3] Reduced uptake of apoptotic cells by macrophages in systemic lupus erythematosus: correlates with decreased serum levels of complement [J].

Bijl, M ;

Reefman, E ;

Horst, G ;

Limburg, PC ;

Kallenberg, CGM .

ANNALS OF THE RHEUMATIC DISEASES, 2006, 65 (01) :57-63

[4] Links between complement deficiency and apoptosis [J].

Botto, M .

ARTHRITIS RESEARCH, 2001, 3 (04) :207-210

[5] Impaired recognition of apoptotic neutrophils by the C1q/calreticulin and CD91 pathway in systemic lupus erythematosus [J].

Donnelly, Suzanne ;

Roake, Wendy ;

Brown, Simon ;

Young, Philip ;

Naik, Haley ;

Wordsworth, Paul ;

Isenberg, David A. ;

Reid, Kenneth B. M. ;

Eggleton, Paul .

ARTHRITIS AND RHEUMATISM, 2006, 54 (05) :1543-1556

[6] After shrinkage apoptotic cells expose internal membrane-derived epitopes on their plasma membranes [J].

Franz, S. ;

Herrmann, K. ;

Fuehrnrohr, B. ;

Sheriff, A. ;

Frey, B. ;

Gaipl, U. S. ;

Voll, R. E. ;

Kalden, J. R. ;

Jaeck, H. -M. ;

Herrmann, M. .

CELL DEATH AND DIFFERENTIATION, 2007, 14 (04) :733-742

[7] Lectins detect changes of the glycosylation status of plasma membrane constituents during late apoptosis [J].

Franz, S ;

Frey, B ;

Sheriff, A ;

Gaipl, US ;

Beer, A ;

Voll, RE ;

Kalden, JR ;

Herrmann, M .

CYTOMETRY PART A, 2006, 69A (04) :230-239

[8] 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

[9]

GRESHAM HD, 1991, J IMMUNOL, V146, P3911

[10]

GROSSMAYER GE, 2007, ANN RHEUM DIS 1228

← 1 2 3 4 →