EN PL
ORIGINAL PAPER
Antibodies against protective molecules in systemic lupus erythematosus
 
More details
Hide details
 
Online publication date: 2010-04-08
 
 
Reumatologia 2009;47(6):323-328
 
KEYWORDS
ABSTRACT

Background: Many experiments in vitro and in vivo show that, in patients with SLE, there is impairment in the clearance of apoptotic cells. This leads to prolonged exposure of autoantigens to the immune system and to autoimmunity.
The aim of the study was to investigate the relationship between antibodies against protective molecules and the activity of lupus measured by the SLEDAI scale.
Material and methods: 45 lupus patients were assessed for the presence of protective molecules in lupus and antibodies against these molecules.
Results: Levels of hsCRP and anti-C1q were higher in SLE patients compared to the control group, whereas the level of MBL was statistically lower in the SLE group. There was no correlation between levels of hsCRP, MBL, C1q, C4, anti-C1q or anti-CRP in patients and the activity of the disease.
Conclusions: CRP plays the most important role in the clearance of apoptotic material in SLE, and therefore is protective in lupus. The lower levels of MBL in patients with SLE suggest its protective value in this disease. There was low incidence of the presence of assessed antibodies, and therefore there was no possibility to evaluate their role in SLE.
 
REFERENCES (27)
1.
Jacobson DL, Gange SJ, Rose NR, Graham NM. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin Immunol Immunopathol 1997; 84: 223-243. .
 
2.
Cooper GS, Dooley MA, Treadwell EL, et al. Hormonal, environmental, and infectious risk factors for developing systemic lupus erythematosus. Arthritis Rheum 1998; 41: 1714-1724. .
 
3.
Majno G, Joris I. Apoptosis, oncosis, and necrosis. An overview of cell death. Am J Pathol 1995; 146: 3-15. .
 
4.
Skulachev VP. Programmed death phenomena: from organelle to organism. Ann N Y Acad Sci 2002; 959: 214-237. .
 
5.
Bijl M, Limburg PC, Cees GM, Kahlenberg CG. New insights into the pathogenesis of systemic lupus erythematosus (SLE): the role of apoptosis. Neth J Med 2001; 59: 66-75. .
 
6.
Cohen JJ. Apoptosis. Immunol Today 1993; 959: 126-130. .
 
7.
Savill J, Fadok V. Corpse clearance defines the meaning of cell death. Nature 2000; 407: 784-788. .
 
8.
Sheriff A, Gaipl US, Voll RE, et al. Apoptosis and systemic lupus erythematosus. Rheum Dis Clin North Am 2004; 30: 505-527. .
 
9.
Bennett L, Palucka AK, Arce E, et al. Interferon and granu-lopoesis signatures in systemic lupus erythematosus blood. J Exp Med 2003; 197: 711-723. .
 
10.
Cohen JJ, Duke RC, Fadok VA, et al. Apoptosis and programmed cell death and immunity. Ann Rev Immunol 1992; 10: 267-293. .
 
11.
Casciola-Rosen LA, Anhalt G, Rosen A. Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes. J Exp Med 1994; 179: 1317-1330. .
 
12.
Kavai M. Immune complex clearance by complement receptor type 1 in SLE. Autoimmun Rev 2008; 8: 160-164. .
 
13.
Kavai M, Szegedi G. Immune complex clearance by monocytes and macrophages in systemic lupus erythematosus. Auto-immun Rev 2007; 6: 497-502. .
 
14.
Katsiari CG, Liossis SN, Sfikakis PP. The Pathophysiologic Role of Monocytes and Macrophages in Systemic Lupus Erythematosus: A Reappraisal. Semin Arthritis Rheum 2009; 14 [Epub ahead of print]. .
 
15.
Chang MK, Binder CJ, Torzewski M, et al. C-reactive protein binds to both oxidized LDL and apoptotic cells through recogni-tion of a common ligand: Phosphorylcholine of oxidized phospholipids. Proc Natl Acad Sci U S A 2002; 99: 13043-13048. .
 
16.
Ciurana CL, Hack CE. Competitive binding of pentraxins and IgM to newly exposed epitopes on late apoptotic cells. Cell Immunol 2006; 239: 14-21. .
 
17.
Gershov D, Kim S, Brot N. C-reactive protein binds to apoptotic cells, protects the cels from assembly of the terminal complement components, and sustains an antiinflammatory innate immune response. Implications for systemic autoimmunity. J Exp Med 2000; 192: 1353-1364. .
 
18.
Takahashi, Tsutsumi A, Ohtani K, et al. Association of mannose binding lectin (MBL) gene polymorphism and serum MBL concentration with characteristics and progression of systemic lupus erythematosus. Ann Rheum Dis 2005; 64: 311-314. .
 
19.
Boniotto M, Braida L, Baldas V, et al. Evidence of a correlation between mannose binding lectin and celiac disease: a model for other autoimmune diseases. J Mol Med 2005; 83: 308-315. .
 
20.
James JA, Kaufman KM, Farris AD, et al. An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythema-tosus. J Clin Invest 1997; 100: 3019-3026. .
 
21.
Schoenfeld Y, Szyper-Kravitz M, Witte T, et al. Autoantibodies against protective molecules – C1q, C-reactive protein, serum amyloid P, mannose-binding lectin, and apolipoprotein A1 prevelence in systemic lupus erythematosus. Ann NY Acad Sci 2007; 1108: 227-239. .
 
22.
Rosenau BJ, Schur PH. Antibodies to C-reactive protein. Ann Rheum Dis 2006; 65: 674-676. .
 
23.
Moroni G, Trendelenburg M, Del Papa N, et al. Anti-C1q antibodies may help in diagnosing a renal flare in lupus nephritis. Am J Kidney Dis 2001; 37: 490-498. .
 
24.
Trouw LA, Daha MR. Role of anti-C1q autoantibodies in the pathogenesis of lupus nephritis. Expert Opin Biol Ther 2005; 5: 243-251. .
 
25.
Daha MR. Pathogenic role of auto-antibodies against complement components in systemic lupus erythematosus. Lupus 2008; 17: 385-388. .
 
26.
Coremans IE, Spronk PE, Bootsma H, et al. Changes in antibodies to C1q predict renal relapses in systemic lupus erythematosus. Am J Kidney Dis 1995; 26: 595-601. .
 
27.
Mosca M, Chimenti D, Pratesi F, et al. Prevalence and clinico-serological correlations of anti-alpha-enolase, anti-C1q, and anti-dsDNA antibodies in patients with systemic lupus erythematosus. J Rheumatol 2006; 33: 695-697.
 
Copyright: © Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie. This is an Open Access journal, all articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (https://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
eISSN:2084-9834
ISSN:0034-6233
Journals System - logo
Scroll to top