Erythrocyte CR1 Determination Using Monoclonal Antibody in a Microtiter Plate ELISA; Receptors Are Not Masked by Immune Complexes

Thomsen, B.; Nielsen, Henry; Bendixen, Gunnar

doi:10.1111/j.1398-9995.1986.tb00332.x

Cited by 13 publications

(17 citation statements)

References 30 publications

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“…Erythrocytes from 42 patients of each genotype (randomly selected regardless of disease severity) were measured by a microtiter plate ELISA 17 with modifications. 18 Briefly, erythrocyte samples were washed 3 times and suspended in phosphate buffered saline. In order to adjust the amount of erythrocytes applied into each well, 100 l of the suspension was lysed in 3.4 ml of distilled water.…”

Section: Methodsmentioning

confidence: 99%

“…On the other hand, the elevation of serum creatinine level in the severe group was moderate, probably resulted from reduced renal blood flow 25 and increased protein catabolism due to pyrexia. 18 CR1 density polymorphism. The frequencies of each genotype in the severe malaria group, uncomplicated malaria group, and healthy individuals are shown in Table 2.…”

Section: Patient Characteristicsmentioning

confidence: 99%

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CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand.

Nagayasu

Ito²,

Akaki³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

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Abstract. Complement receptor type 1 (CR1) on erythrocytes shows an inherited numerical polymorphism which correlates with a HindIII-RFLP (restriction fragment length polymorphism) of the CR1 gene in various populations. To investigate the relationship between CR1 density polymorphism and disease severity, we typed 185 Thai patients with acute falciparum malaria (55 severe and 130 uncomplicated) for their genotypes of this polymorphism. The level of expression of erythrocyte CR1 from 42 randomly selected patients was measured by enzyme-linked immunosorbent assay (ELISA). We observed a significantly higher frequency of homozygotes of the CR1 low density allele (LL) among the severe group as compared to the uncomplicated group (P ϭ 0.005). CR1 expression on erythrocytes from patients with the LL genotype was significantly lower than homozygotes with the high density allele (HH) (P Ͻ 0.0001) and heterozygotes (HL) (P ϭ 0.013). The results suggest that a genetically-determined low CR1 density on erythrocytes may be a risk factor for developing a more severe form of malaria in Thai subjects.

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Section: Methodsmentioning

confidence: 99%

Section: Patient Characteristicsmentioning

confidence: 99%

CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand.

Nagayasu

Ito²,

Akaki³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

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“…TT-aTT were first allowed to bind to RBC at optimized conditions (30). It is shown that the factor 1 inhibitor suramin inhibits release in the presence of EDTA.…”

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confidence: 99%

“…The CRl levels were determined by the microtiter plate ELISA (30). The CRl levels were determined by the microtiter plate ELISA (30).…”

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confidence: 99%

Release of Immune Complexes Bound to CR1 on Erythrocytes; Suramin Inhibits Factor I in the Presence of EDTA

Thomsen

Nielsen

Bendixen

1986

Allergy

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An experimental model was established in order to study the release of immune complexes (IC) bound by complement C3b receptors (CR1) on human erythrocytes (RBC). Soluble tetanus toxoid anti-tetanus toxoid complexes were incubated with RBC in the presence of autologous serum at optimal conditions for binding. The RBC carrying complement-opsonized complexes were incubated with appropriate serum reagents, and it was shown that factor I was required for release of the complexes, which occurred without loss of CR1. Suramin was, irrespective of factor I, found to induce release of CR1-bound IC in the absence of EDTA, whereas factor I-mediated release was inhibited by suramin in the presence of EDTA. EDTA probably interfered through a charge-dependent interaction. These observations are decisive for the interpretation of in vitro experiments involving these reagents. The combination of EDTA and suramin was found inappropriate for use in quantitative determination of in vivo CR1-bound IC.

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“…Blockade by ICs is not the answer; counting methods independent of CRl occupancy have been used (38,56), and Taylor and colleagues (57) have shown that ICs bound to erythrocytes in vivo can be detected in only a few patients with SLE. Similarly, autoantibodies to CRl have been demonstrated in only a very small group of cases (58,59).…”

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confidence: 99%

Untitled

1988

Arthritis & Rheumatism

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The existence of a complement receptor on erythrocytes of primates and on platelets of other vertebrates has been a scientific curiosity for many years. The attention of investigators studying the pathophysiology of diseases mediated by immune complexes (ICs) has recently been drawn to this receptor, complement receptor type 1 (CRI), by a number of studies that have characterized some of the probable physiologic activities of CRI.Binding reactions of microorganisms to platelets were first observed by Bull in 1915 (1) and by Rieckenberg in 1917 (2). Rieckenberg observed that the sera of rats that had recovered from infection with Trypanosoma brucei would cause blood platelets to adhere to T brucei in vitro. The role of complement in mediating these binding reactions was initially suggested by Kritschewsky and Tscherikower (3) A similar binding reactivity was first recognized on primate erythrocytes by workers studying the serologic reactivities of trypanosomes. These would adhere to human erythrocytes in the presence of typespecific antiserum and complement (8). This specific adherence reaction provided a simple technique for serotyping trypanosomes. Variation in the ability of erythrocytes from dieerent donors to support immune adherence was noted by Brown and Broom (7). Brown's own erythrocytes consistently failed to show any binding to opsonized trypanosomes, whereas Broom's erythrocytes showed strong adherence. This phenotypic difference was stable for more than 2 years. They also compared 52 samples of red blood cells from patients with various diseases with samples from 26 normal subjects. Although no overall difference was noted between the 2 groups in the prevalence of nonadherent erythrocytes, it is interesting to note that specimens from 2 patients with tuberculosis and 1 patient with "subacute rheumatism" showed no adherence. These early observations were published mainly in French and German, and in British journals of tropical medicine, and were overlooked between the late 1930s and early 1950s.In 1953, R. A. Nelson (9) initiated the next phase of CRl research when he re-described binding reactions between human erythrocytes and specifically opsonized treponemes and pneumococci, and coined the term "immune adherence" to describe the reaction. The detailed biochemical characterization of

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Erythrocyte CR1 Determination Using Monoclonal Antibody in a Microtiter Plate ELISA; Receptors Are Not Masked by Immune Complexes

Cited by 13 publications

References 30 publications

CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand.

CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand.

Release of Immune Complexes Bound to CR1 on Erythrocytes; Suramin Inhibits Factor I in the Presence of EDTA

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