Immune complex processing in patients with systemic lupus erythematosus. In vivo imaging and clearance studies.

Davies, Kevin; Peters, Anke; Beynon, Huw; Walport, Mark J.

doi:10.1172/jci116090

Cited by 142 publications

(104 citation statements)

References 31 publications

(20 reference statements)

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“…Auto-antibodies against C1q are directed against a highly functional molecule that plays important roles in preventing autoimmunity [39][40][41]. Here, we show a strong correlation between the occurrence of anti-C1q antibodies, up-regulation of BAFF, consumption of C1q, and elevated levels of sVCAM-1 in children with active LN.…”

Section: Discussionmentioning

confidence: 50%

Markers of childhood lupus nephritis indicating disease activity

et al. 2010

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Current treatment regimens for childhood lupus nephritis (LN) are associated with significant side-effects and toxicity in vulnerable phases of growth and development. The paucity of biomarkers particularly in childhood impedes the appropriate clinical management and the development of new therapeutics. We analyzed markers of immune system (BAFF, RANTES), complement (Bb, C1q, C3d-CIC, C5a) and endothelial cell activation (sVCAM-1) in children with LN (n=22, mean age 14.8±4.7 years), nephrotic syndrome (n =13) and age-matched healthy controls (n=20) to define parameters that correlate with LN activity. Complement fragments of the alternative (Bb, p=0.0004) classical (C3d-CIC, p<0.0001) and common pathway (C5a, p<0.0001) and the levels of BAFF (p< 0.0001), RANTES (p=0.0002) and sVCAM-1 (p=0.0004) were significantly higher in active compared to inactive LN. Activation of complement was associated with the occurrence of anti-C1q antibodies and reduced complement

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Section: Discussionmentioning

confidence: 50%

Markers of childhood lupus nephritis indicating disease activity

et al. 2010

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“…Future work should focus on development of more efficient approaches for measuring CN at FCGR3B, replication of this association and investigation of association in clinically-defined subgroups. Given the role of this receptor in the uptake of IC and the fact that impaired clearance of autoantibodies is strongly implicated in the pathogenesis of SLE, 19 it is possible that a similar deficiency contributes to the development of SSc. This association also adds to the list of diseases in which FCGR3B CN has been implicated, suggesting that FCGR3B may be a common autoimmune-related locus.…”

Section: Discussionmentioning

confidence: 99%

Evidence that deletion at FCGR3B is a risk factor for systemic sclerosis

et al. 2012

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There is increasing evidence that gene copy number (CN) variation influences clinical phenotype. The low-affinity Fc receptor 3B (FCGR3B) located in the FCGR gene cluster is a CN polymorphic gene involved in the recruitment of polymorphonuclear neutrophils to sites of inflammation and their activation. Given the genetic overlap between systemic lupus erythematosus and systemic sclerosis (SSc) and the strong evidence for FCGR3B CN in the pathology of SLE, we hypothesised that FCGR3B gene dosage influences susceptibility to SSc. We obtained FCGR3B deletion status in 777 European Caucasian cases and 1000 controls. There was an inverse relationship between FCGR3B CN and disease susceptibility. CN of p1 was a significant risk factor for SSc (OR ¼ 1.55 (1.13-2.14), P ¼ 0.007) relative to CNX2. Although requiring replication, these results suggest that impaired immune complex clearance arising from FCGR3B deficiency contributes to the pathology of SSc, and FCGR3B CN variation is a common risk factor for systemic autoimmunity.

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“…The strongest disease susceptibility genes for the development of SLE which have been identified to date are null alleles of genes encoding proteins of the classical pathway of complement activation [11]. It has been postulated that complement deficiency may predispose to the disease as a consequence of impairment of the processing of immune complexes, and there is direct experimental evidence, obtained from the study of immune complex processing in patients with SLE, that this is the case [12]. However, Fc receptors are also of major importance in immune complex processing, and there is evidence from the study of the clearance of IgG-opsonized erythrocytes in SLE patients that Fc-receptor function in SLE may be impaired [2].…”

Section: Discussionmentioning

confidence: 99%

FcγRIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease

Botto¹,

Theodoridis²,

Thompson

et al. 1996

Clinical and Experimental Immunology

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109

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SUMMARYAn allotypic variant of Fc°RIIa, Fc°RIIa-HR (Fc°RIIa-R131), has been shown in vitro to reduce the capacity of phagocytic cells to bind and internalize IgG-containing immune complexes. Our aim was to determine whether this allotypic variant was associated with susceptibility to SLE and the development of lupus nephritis, as previous studies have suggested. Fc°RIIA genotype analysis was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) in 215 Caucasoid, 70 Afro-Caribbean, and 46 Chinese patients with SLE, and in 259, 77, and 49 ethnically matched controls, respectively. Distribution of Fc°RIIa genotypes between the patients and ethnically matched controls was not significantly different in the three populations studied. No association between the Fc°RIIa-HR allotype and nephritis was found. Our results suggest that the Fc°RIIa-HR allotype is not a major factor predisposing to the development of SLE, or to lupus nephritis.

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Immune complex processing in patients with systemic lupus erythematosus. In vivo imaging and clearance studies.

Cited by 142 publications

References 31 publications

Markers of childhood lupus nephritis indicating disease activity

Markers of childhood lupus nephritis indicating disease activity

Evidence that deletion at FCGR3B is a risk factor for systemic sclerosis

FcγRIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease

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