Fixation of C3 to Platelets in Vitro by Antiplatelet Antibody from Patients with Immune Thrombocytopenic Purpura

McMillan, Robert; Martin, Meghan

doi:10.1111/j.1365-2141.1981.tb02786.x

Cited by 36 publications

(15 citation statements)

References 12 publications

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“…In vitro studies have given convincing evidence that platelets may fix complement C3 in presence of antiplatelet antibodies [28]. Thus, the rate of elevated PAC3 of 24% in this study is in line with our previous report [ 161.…”

Section: Discussionsupporting

confidence: 93%

Platelet‐associated immunoglobulins IgG, IgM, IgA and complement C3 in immune and nonimmune thrombocytopenic disorders

Panzer

Szamait²,

Bödeker

et al. 1986

American J Hematol

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A two-stage radioactive antiglobulin test--using unlabelled antisera specific for IgG, IgA, IgM and C3 followed by binding of 125I-staphylococcal protein A--was applied to determine platelet-associated immunoglobulins (PAIg) and complement (PAC3) in thrombocytopenias of various etiologies. One hundred and one patients with immune thrombocytopenia (chronic autoimmune, 48; acute autoimmune, 37; Evans syndrome, nine; connective tissue diseases, seven) and 20 patients with presumed nonimmune thrombocytopenia (bone marrow aplasia or malignancy, six; septicemia, five; hypersplenism, five; cirrhosis of liver, three; others, one) were studied. Increased levels of PAIg/C3 were found in 76% of patients with immune thrombocytopenia. PAIgG was raised in 66%, PAIgM in 57%, PAIgA in 44%, and PAC3 in 29%. Isolated elevation of PAIgG and of PAIgM was found in four and three cases, respectively; PAIgA and PAC3 were elevated in one case each. PAIgG was associated with PAIgM in 56%, with PAIgA in 34%, and with PAC3 in 27%. Both patients with Evans' syndrome and patients with connective tissue diseases had significantly higher PAIgM levels than the other patients with immune thrombocytopenia. In patients with nonimmune thrombocytopenia, increased rates of PAIg/C3 were also encountered. Positive test results were found in 88% (PAIgG 88%, PAIgM 47%, PAIgA 35%, and PAC3 24%). In immune-mediated thrombocytopenia, we observed a significant inverse correlation between platelet counts and PAIgG, PAIgA, and PAC3, but not with PAIgM. In contrast, no such correlation was found in patients with nonimmune thrombocytopenia. Our data indicate that the evaluation of neither parameter alone nor the combination of PAIg/C3 will discriminate between immune and nonimmune thrombocytopenia. Preferential coating with certain immunoglobulins, however, may be present in some subgroups of immune thrombocytopenias.

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Section: Discussionsupporting

confidence: 93%

Platelet‐associated immunoglobulins IgG, IgM, IgA and complement C3 in immune and nonimmune thrombocytopenic disorders

Panzer

Szamait²,

Bödeker

et al. 1986

American J Hematol

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“…TNT003 appears to impact CP activation predominantly downstream of C1 binding, and supports the notion that CP activation plays a major role in terminal complement pathway activation in ITP plasma. Indeed, in vitro platelet lysis has been described following normal platelet exposure to autoantibodies from ITP patient sera (McMillan, et al 1981). …”

mentioning

confidence: 99%

Classical complement pathway activation in immune thrombocytopenia purpura: inhibition by a novel C1s inhibitor

Peerschke

Panicker²,

Bussel

2015

Br J Haematol

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“…McMillan and Martin [26] showed that incubation of target platelets with purified IgG synthesized by splenic cells from ITP patients resulted in fixation of C3. Hauch and Rosse [ 131 found 56 % of patients with immune thrombocytopenia to have increased PA-C3, but in no case was PA-C3 increased in the absence of increased PA-IgG.…”

Section: Discussionmentioning

confidence: 99%

Use of the indirect platelet radioactive antiglobulin test with anti‐IgG and anti‐C3 in immune and nonimmune thrombocytopenias

1985

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Indirect platelet radioactive antiglobulin tests using anti-IgG and anti-C3 were performed in 483 individuals. The subjects' diagnoses and clinical states were correlated with sensitizing protein ( IgG and/or C3). Sensitivity of the technique was increased by increasing the serum to cell ratio and there was good Correlation between direct and indirect antiglobulin tests in 56 patients. Seven percent of normal healthy nonthrombocytopenic untransfused males and 88 % of patients in whom autoimmune thrornbocytopenia was clinically suspected showed a positive test result. In the indirect antiglobulin test, mean f SD fg anti-C3d/platelet was 1.75 f 0.28 (N = 58) with serum from normal subjects, 3.91 f 1.86 (N = 123) with serum from patients with idiopathic thrombocytopenic purpura and systemic lupus erythematosus, and 2.78 f 0.91 (N = 52) with serum from patients with lymphoproliferative disease.The differences were significant with P < 0.001. Levels of bound anti-IgG were in general accord with those of other reports; there was no significant relationship with serum immunoglobulin levels. When the indirect antiglobulin tests were positive for both IgG and C3, there was a significant correlation between IgG and C3 bound to normal platelets (r = 0.671; P < 0.01). Although sera from 39% of patients whose thrombocytopenia was not initially suspected to be on an autoimmune basis gave a positive test result, indirect platelet radioactive antiglobulin tests using anti-IgG and anti-C3 may be convenient tools in the evaluation and follow-up of immune thrombocytopenias.

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Fixation of C3 to Platelets in Vitro by Antiplatelet Antibody from Patients with Immune Thrombocytopenic Purpura

Cited by 36 publications

References 12 publications

Platelet‐associated immunoglobulins IgG, IgM, IgA and complement C3 in immune and nonimmune thrombocytopenic disorders

Platelet‐associated immunoglobulins IgG, IgM, IgA and complement C3 in immune and nonimmune thrombocytopenic disorders

Classical complement pathway activation in immune thrombocytopenia purpura: inhibition by a novel C1s inhibitor

Use of the indirect platelet radioactive antiglobulin test with anti‐IgG and anti‐C3 in immune and nonimmune thrombocytopenias

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