1981
DOI: 10.1111/j.1365-2141.1981.00069.x
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Quantitation of Red Blood Cell‐bound C3d in Normal Subjects and Random Hospitalized Patients

Abstract: Summary. A sensitive radiolabelled anti‐antiglobulin method was devised and applied to quantitating red blood cell‐bound C3d (RBC‐C3d) in samples from 174 normal blood donors. C3d was demonstrable on all RBC examined; 98% of values fell over a broad range, with the highest values being approximately 3·5 × the lowest values (equivalent to 50–160 molecules of C3d per cell). RBC‐C3d did not correlate with sex or age (over 18–65 years); indirect evidence suggests that values for the paediatric age group will fall … Show more

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Cited by 49 publications
(19 citation statements)
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References 9 publications
(5 reference statements)
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“…17 In contrast to this finding is the fact that several studies of hospitalized patients have demonstrated that almost 10% have positive DATs without any evidence of hemolysis. 3,5,[18][19][20] However, in most instances, the DATs were very weakly reactive, 1+ or less, and complement alone was detected on the red cells.…”
Section: Discussionmentioning
confidence: 96%
“…17 In contrast to this finding is the fact that several studies of hospitalized patients have demonstrated that almost 10% have positive DATs without any evidence of hemolysis. 3,5,[18][19][20] However, in most instances, the DATs were very weakly reactive, 1+ or less, and complement alone was detected on the red cells.…”
Section: Discussionmentioning
confidence: 96%
“…Small amounts of C3 fragments have previously been detected on E from healthy individuals [4,[9][10][11], while increased amounts of C3d,g have been demonstrated on E from patients with inflammatory diseases, such as SLE or rheumatoid arthritis (RA) [4,[9][10][11]. We observed that all subpopuiations of SLE blood leucocytes, as well as E, carry raised levels of in v/vo-deposited C3d,g, but not C3b or iC3b fragments, compared with normal individuals.…”
Section: Discussionmentioning
confidence: 99%
“…The erythrocytes (E) of many patients with SLE display a relative deficiency of complement receptor (CRl) [1][2][3][4][5][6][7][8] as well as increased deposition of the C3-split product, C3d,g, on the E-membrane [9][10][11][12]. Both inherited [3,7] and acquired [1,4,6] factors have been reported to contribute to the deficiency of E-CRl in SLE patients.…”
Section: Introductionmentioning
confidence: 99%
“…If it deposits on healthy self-tissue or ticks over in the fluid phase, host regulatory proteins immediately inactivate it. Evidence of this AP turnover is that a red blood cell contains on average several hundred C3d fragments covalently bound to its membrane (5). In addition, a small percentage of serum albumin migrates at approximately 100 kDa, not 55, because of the attachment to it of a C3d fragment (6).…”
Section: Complement Pathwaysmentioning
confidence: 99%