Apoptosis, nucleosomes, and nephritis in systemic lupus erythematosus

Tax, W.J.M.; Kramers, C.; Bruggen, M.C.J. van; Berden, J.H.M.

doi:10.1038/ki.1995.336

Cited by 97 publications

(68 citation statements)

References 64 publications

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“…Decreased clearance of apoptotic cells results in prolonged exposure of these cell surface-expressed autoantigens to the immune system in SLE, which might explain why autoantibodies against these intracellular antigens develop. Disturbance in the clearance of apoptotic cells, therefore, is considered one of the pathophysiologic mechanisms underlying the breakdown of tolerance and, subsequently, the induction of SLE (9).…”

Section: Conclusion Autoantibodies From Sle Patients Are Able To Opsmentioning

confidence: 99%

Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism

Reefman¹,

Horst²,

Nijk³

et al. 2007

Arthritis & Rheumatism

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Objective. Decreased clearance of apoptotic cells is suggested to be a major pathogenic factor in systemic lupus erythematosus (SLE). The aim of this study was to investigate whether the binding of SLE autoantibodies to apoptotic cells influences the phagocytosis of these cells by macrophages. Conclusion. Autoantibodies from SLE patients are able to opsonize apoptotic cells and inhibit their uptake by macrophages via an Fc␥R-dependent mechanism. Methods. Apoptosis was induced in a human

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Section: Conclusion Autoantibodies From Sle Patients Are Able To Opsmentioning

confidence: 99%

Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism

Reefman¹,

Horst²,

Nijk³

et al. 2007

Arthritis & Rheumatism

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show abstract

“…These facts must be taken into account in in vitro studies involving such materials: the formation of complexes may bias the screening procedure; it may also impair the characterization of its paratopic and idiotypic specificities or its physicochemical characterization by electrofocusing. The presence of such complexes should also be considered in in vivo experiments, since nucleosomes are likely to be involved in the induction of autoimmunity and in the development of glomerular lesions [1,2].…”

Section: Discussionmentioning

confidence: 99%

“…In vivo, DNA is associated to histones in the nucleosomal subunit of chromatin. In lupus, nucleosomes could be at work in the induction of anti-DNA antibodies [1], and in the development of kidney lesions [2]. Recent observations suggest that cationic residues of histones could bind to anionic heparan sulphate and mediate the glomerular deposition of autoantibodies.…”

Section: Introductionmentioning

confidence: 99%

Detection of nucleosome–IgG immune complexes in ascites from mice transplanted with anti-DNA antibody-secreting hybridomas and in plasmas from MRL-lpr/lpr mice

Fournié

1996

Clinical and Experimental Immunology

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SUMMARYAutoantibodies directed against chromatin components characterize lupus diseases. Immune complexes made of these autoantibodies bound to nucleosomes released from dead cells could play some pathogenic role. The aims of this study were to investigate if nucleosome-IgG complexes could contaminate IgG anti-DNA MoAb preparations, and if such complexes circulate in lupus diseases. A new method was set up using preformed nucleosome-IgG complexes. Complexes were adsorbed onto microplate through Fc binding and nucleosomal DNA was detected by internal incorporation of labelled nucleotide. Using this method, high amounts of complexes were found in ascites from mice transplanted with anti-DNA antibody-secreting hybridomas. In some ascites, nucleosome was found to be strongly associated with the MoAb, confirming that nucleosome-IgG complexes could contaminate monoclonal autoantibody preparations. In MRL-lpr/lpr mice, nucleosome-IgG complexes were detected at 16-24 weeks of age at a time when kidney lesions are rapidly worsening, raising the question of their pathogenic significance.

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“…In effect, autoreactivity has been recognized against antigens present in apoptotic cells (155). If apoptotic cells are not adequately cleared, their contents might be released and further stimulate this autoimmune response (156). It has been suggested that this may help explain the relationship between infection and the initiation/exacerbation of autoimmunity, as infection can trigger apoptosis (4).…”

Section: Apoptosis and The Immune Responsementioning

confidence: 99%

Apoptosis in renal diseases

Egido¹

1996

Front Biosci

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Apoptosis, nucleosomes, and nephritis in systemic lupus erythematosus

Cited by 97 publications

References 64 publications

Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism

Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism

Detection of nucleosome–IgG immune complexes in ascites from mice transplanted with anti-DNA antibody-secreting hybridomas and in plasmas from MRL-lpr/lpr mice

Apoptosis in renal diseases

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