The Raji cell radioimmune assay for detecting immune complexes in human sera.

Theofilopoulos, Argyrios N.; Wilson, Curtis B.; Dixon, Frank J.

doi:10.1172/jci108257

Cited by 652 publications

(202 citation statements)

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“…Raji cell radioimmunoassay (RCA) was performed by the technique of Theofilopoulos et a1 (9). In our laboratory, sera of normal donors (50 individuals tested) yield control values of 47 ?…”

Section: Methodsmentioning

confidence: 99%

“…In the present study, sera of 92 unselected patients with PSS were examined for the presence of immune complexes by three techniques: the Raji cell radioimmunoassay (RCA) (9), the Clq binding assay (ClqBA) (lo), and pattern recognition on agarose gel electrophoresis (AGE) (1 1). Correlations with clinical and other laboratory features of PSS were sought by computer analysis of an extensive database compiled on these patients in our center as part of the American Rheumatism Association Medical Information System (ARAMIS) (12).…”

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confidence: 99%

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Immune complexes in progressive systemic sclerosis (scleroderma)

Seibold

Medsger

Winkelstein

et al. 1982

Arthritis & Rheumatism

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Serum immune complexes were measured in 92 patients with progressive systemic sclerosis, and elevated levels were found as follows: Raji cell assay 72% (59% after pronase treatment of Raji cells), agarose gel electrophoresis 52%, and Clq binding 24%. Fortythree (47%) had abnormal results on two or more of these tests, but only 17 (18%) had normal results by all three assays. Computer-assisted analysis of immune complex results and extensive clinical and laboratory data compiled on these patients revealed that the patients with abnormal Raji cell assays more often had diffuse scleroderma, tendon friction rubs, and positive serum antinuclear antibody tests than did patients with negative results on Raji cell assays. Individuals with immune complexes detected by Clq binding had evi- dence of pulmonary involvement and positive serum rheumatoid factor more frequently than did patients whose Clq tests were negative.The etiology of progressive systemic sclerosis (PSS, scleroderma) is unknown. Any hypothesis concerning the pathogenesis of this disease must account for both the prominence of vascular lesions in involved tissues (1,2) and the high frequency of abnormal serologic and cellular immune reactions (3). Initiation or mediation of vascular damage by circulating immune complexes might satisfy these requirements. In reports to date on immune complexes in PSS, investigators have studied small groups of patients and used a variety of immune complex assays, with contradictory results (4-8).In the present study, sera of 92 unselected patients with PSS were examined for the presence of immune complexes by three techniques: the Raji cell radioimmunoassay (RCA) (9), the Clq binding assay (ClqBA) (lo), and pattern recognition on agarose gel electrophoresis (AGE) (1 1). Correlations with clinical and other laboratory features of PSS were sought by computer analysis of an extensive database compiled on these patients in our center as part of the American Rheumatism Association Medical Information System (ARAMIS) (12). PATIENTS AND METHODSSelection of patients. Single serum samples from 92 patients with PSS were examined; the group included 68 women and 24 men, ranging in age at study from 18 to 85 years (mean 48.3). Forty-eight of these individuals (32 women, 16 men) had diffuse scleroderma and 44 (36 women, 8 men) had the CREST syndrome (calcinosis, Raynaud's

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“…Raji cell radioimmunoassay (RCA) was performed by the technique of Theofilopoulos et a1 (9). In our laboratory, sera of normal donors (50 individuals tested) yield control values of 47 ?…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Immune complexes in progressive systemic sclerosis (scleroderma)

Seibold

Medsger

Winkelstein

et al. 1982

Arthritis & Rheumatism

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“…A potential role of immune complexes, which have been detected in SLE sera (1)(2)(3)(4), in the development of the inflammatory process in this disease has been emphasized (5)(6)(7). In view of the important role of polymorphonuclear neutrophils (PMN) in the pathogenesis of well established immune complex diseases such as experimental serum sickness (8), it was desirable to investigate possible abnormalities of PMN function in SLE.…”

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confidence: 99%

Increased endothelial cell adherence, aggregation, and superoxide generation by neutrophils incubated in systemic lupus erythematosus and felty's syndrome sera

Hashimoto

Ziff

Hurd

1982

Arthritis & Rheumatism

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The ability of sera from patients with systemic lupus erythematosus (SLE) and Felty's syndrome to induce increased adhesiveness of normal human neutrophils (PMN) was investigated. PMN from normal healthy donors were incubated in sera from 19 patients with active SLE, 12 with inactive SLE, 20 with Felty's, 24 with rheumatoid arthritis, and 34 normal persons. After incubation, the degree of adherence of the PMN to human endothelial cells in culture, their aggregation, and superoxide (O2‐) generation were determined. Sera from patients with both active SLE and Felty's syndrome induced significantly increased PMN adherence to endothelial cells and PMN aggregation in vitro, compared with normal sera. This increased adherence to endothelial cells was maintained after heat treatment (56°C for 30 minutes) of the sera. In O2‐ generation experiments, sera from patients with active SLE induced significantly increased O2‐ release from normal PMN using both fresh and heat‐treated sera. Sera from Felty's patients demonstrated the same effect with heattreated sera but not with fresh sera. When sera from patients with active SLE and Felty's syndrome were used, all three parameters correlated significantly with each other in individual patients. In contrast, sera from the 12 patients with inactive SLE and 24 rheumatoid arthritis patients without Felty's failed to induce significant differences in the three parameters studied when compared with 34 normal controls. Fractionation of 3 SLE sera and 1 Felty's serum on Sephadex G‐200 demonstrated that the adherence enhancing factor was present in both IgG and IgG‐excluded fractions. The observed increased adhesiveness of PMN induced by SLE and Felty's sera may, at least in part, contribute to the neutropenia which is common in these diseases. Increased O2‐ release associated with PMN adherence may contribute to endothelial cell damage and vascular injury, which is also a common manifestation of these diseases.

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“…The occurrence of circulating immune complexes in cancer patients has been suggested first by the demonstration of serum blocking factors possibly related to immune complexes, and secondly by the direct detection of material similar to antigenantibody complexes in some patients with various types of malignancy (18,(20)(21)(22)(23)(24)(25)(26)(27)(28)39). In human leukemia, the presence of immune complexes has been suggested by the finding of renal glomerular deposits of Ig and complement in a few cases (29).…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence that serum blocking factors may consist of immune complexes (16)(17)(18)(19). Furthermore, several studies have indicated that antigen-antibody complexes, possibly related to the tumor, may circulate in blood (18,(20)(21)(22)(23)(24) or be deposited in tissues (25)(26)(27)(28) of patients with different types of malignancy, including leukemia (29 The present study was carried out, using the [125I]-Clq-binding test (30) and the Raji cell radioassay (23), to determine the incidence of circulating immune complexes in leukemia and to investigate their relationship to clinical and biological features of the disease and to prognosis. The serum Clq-binding material which was detected was further characterized by immunochemical and physical analysis.…”

Section: Introductionmentioning

confidence: 99%