Interaction between immune complexes and C3b receptors on erythrocytes

Yoshida, Kenji; Yukiyama, Yasushi; Miyamoto, Tomofumi

doi:10.1016/0090-1229(86)90085-1

Cited by 11 publications

(6 citation statements)

References 10 publications

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“…The Erythrocyte CR1 (ECR1) is able to bind to C3b/C4b opsonized immune complexes (Yoshida et al, 1986) and localize them on the erythrocytic membrane ( Fig. 2A).…”

Section: Clearance Of Immune Complexesmentioning

confidence: 99%

Complement Receptor 1: Disease associations and therapeutic implications

Khera

Das

2009

Molecular Immunology

170

128

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Exaggerated complement activation is a key event in the pathogenesis of a range of autoimmune and inflammatory diseases. Complement Receptor 1 (CR1) has emerged as a molecule of immense interest in gaining insight to the susceptibility, pathophysiology, diagnosis, prognosis and therapy of such diseases. This review brings forth a composite view of the current understanding on the structure, functions, genetics, disease associations and therapeutic implications of CR1.

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“…The Erythrocyte CR1 (ECR1) is able to bind to C3b/C4b opsonized immune complexes (Yoshida et al, 1986) and localize them on the erythrocytic membrane ( Fig. 2A).…”

Section: Clearance Of Immune Complexesmentioning

confidence: 99%

Complement Receptor 1: Disease associations and therapeutic implications

Khera

Das

2009

Molecular Immunology

170

128

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“…Subendothelially located deposits of modified LDL are likely to induce antibody and LDL-IC formation in situ, and these LDL-ICs are likely to exist as large aggregates, equivalent to insoluble ICs prepared in vitro. Soluble LDL-ICs present in circulation, however, are likely to be formed in antigen excess, and they will tend to be adsorbed to erythrocytes via C3b receptors and other nonspecific interactions (35,36). The erythrocyte-adsorbed ICs are easily transferred to phagocytic cells expressing Fclty receptors of higher affinity, without damage to the erythrocyte (37).…”

Section: Ldl-ics and Macrophagesmentioning

confidence: 99%

Cytokines, Modified Lipoproteins, and Arteriosclerosis in Diabetes

Lopes‐Virella

Virella²

1996

Diabetes

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Modified lipoproteins, particularly different forms of oxidized LDL (ox-LDL), have been reported to elicit humoral immune responses both in experimental animals and humans. In diabetes, glycation and oxidation processes coexist and lead to the formation of glycoxidation products. Ox-LDL has been demonstrated in atheromatous lesions, anti-ox-LDL antibodies have been detected in circulation and in atheromatous plaques, and immune complexes (ICs) formed with LDL and anti-LDL (LDL-IC) have been isolated from the serum of patients with manifestations of atherosclerosis. In addition, in vitro formed LDL-ICs and ICs isolated from patients have been demonstrated to cause intracellular accumulation of cholesteryl esters (CEs) in human macrophages and fibroblasts. The accumulation of CEs in macrophages exposed to LDL-ICs is unique to this type of IC and is associated with paradoxical overexpression of LDL receptor and with increased synthesis and release of interleukin 1 beta and tumor necrosis factor (TNF) alpha. The overexpression of LDL receptors is higher in LDL-IC-stimulated macrophages that release markedly high amounts of TNF-alpha than in macrophages that release low amounts of TNF-alpha into the medium. The release of cytokines in the subendothelial space may have a significant role in promoting the interaction of endothelial cells with mononuclear cells, causing endothelial cell damage directly or indirectly, and also in inducing smooth muscle cell proliferation. Thus, in view of the above data, it can be concluded that humoral autoimmunity may play a significant role in the pathogenesis of atherosclerosis in diabetes.

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confidence: 99%

“…29,30 In addition, CR1 plays a role in the clearance of immune complexes and in phagocytosis. [31][32][33] Thus, the lower levels of CR1 expression on the red cell surface associated with the H/L and L/L genotypes 22 are expected to result in increased complement activation and C3 binding on PNH red cells.In order to test this hypothesis we investigated the kinetics of C3 binding to GPI-negative red cells in vitro 13,14 from patients with the three CR1 HindIII genotypes. When GPI-negative red cells were exposed to activated complement in the presence of eculizumab, we promptly detected C3-positive PNH red cells, the percentage of which increased with time.…”

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confidence: 99%

Polymorphism of the complement receptor 1 gene correlates with the hematologic response to eculizumab in patients with paroxysmal nocturnal hemoglobinuria

et al. 2013

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© F e r r a t a S t o r t i F o u n d a t i o nphic alleles of the C3 gene and of the complement receptor 1 (CR1) gene. Methods PatientsSeventy-two patients with hemolytic PNH who had received eculizumab treatment were analyzed after a median follow-up of 52 months (range, 11-98 months). Patients with evidence of bone marrow failure (reticulocytes ≤60x10 9 /L, platelets ≤50x10 9 /L, neutrophils ≤1x10 9 /L) were not included in this series because this condition may affect the clinical response to eculizumab regardless of how well hemolysis is controlled. Peripheral blood samples were collected for clinical testing, flow cytometry (GPI-molecules and C3-binding) 7 and genotyping after the patients had signed an informed consent form approved by the respective Institutional Review Board. As a criterion of response to eculizumab we used the one that is most stringent and objective: namely RBC transfusion at any time after the first 6 months on eculizumab treatment. Of the 72 patients 60 were transfusiondependent before eculizumab: of these 60, those who on eculizumab received no further transfusion during follow-up have been classified as good responders; those who on eculizumab received one or more RBC transfusion at any time during follow-up have been classified as suboptimal responders. Twelve patients started eculizumab before having received any RBC transfusions. Of these, the ten patients who on eculizumab remained transfusion-independent have been classified as good responders because their hemoglobin level increased, on average, by 2.2 g/dL; the remaining two patients required RBC transfusions on eculizumab and have been classified as sub-optimal responders. Only one patient, who had hemolytic PNH at the time of starting eculizumab and who had already been classified as a sub-optimal responder, became aplastic during follow-up. GenotypingThe polymorphism rs2230199 C>G of the C3 gene was investigated by a newly designed tetra-primer amplification refractory mutation system-polymerase chain reaction method.11 Three polymorphisms of the CR1 gene were genotyped by restriction fragment length (RFLP) analysis:12 HindIII RFLP (intron 27); His1208Arg (exon 22); Pro1827Arg (exon 33). Kinetics of C3 binding in vitroRBC and sera were promptly separated from peripheral blood freshly collected from PNH patients. The RBC were then incubated with sera containing eculizumab as previously described. 13,14 Briefly, a 2% suspension of RBC from PNH patients was incubated at 37°C with a pool of ABO-compatible sera from patients on eculizumab, and the complement alternative pathway was activated by mild acidification (HCl 0.016 M). At serial time points (15,30, 60, and 120 min) after complement activation the fraction of GPI-negative RBC with newly bound C3 fragments was measured by flow cytometry (AccuriC6, Becton Dickinson, NJ, USA) after staining with anti-CD59 Alexa647 (Mem43, Serotec, UK) and anti-C3d-neoantigen (A250, Quidel, CA, USA); secondary staining was performed with phycoerythrin-labeled polyclonal rabbit-an...

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Interaction between immune complexes and C3b receptors on erythrocytes

Cited by 11 publications

References 10 publications

Complement Receptor 1: Disease associations and therapeutic implications

Complement Receptor 1: Disease associations and therapeutic implications

Cytokines, Modified Lipoproteins, and Arteriosclerosis in Diabetes

Polymorphism of the complement receptor 1 gene correlates with the hematologic response to eculizumab in patients with paroxysmal nocturnal hemoglobinuria

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