Activation of human complement by immunoglobulin G antigranulocyte antibody.

Rustagi, Pradip K.; Currie, Mark S.; Logue, Gerald L.

doi:10.1172/jci110712

Cited by 23 publications

(10 citation statements)

References 33 publications

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“…The additional opsonizing activity of complement, activated by antineutrophil autoantibodies, may amplify phagocytosis [7]. Alternatively, the functional status of the phagocytic system may render clearance of the opsonized cells more or less effective [6].…”

Section: Autoimmune Neutropenias: Pathogenesis and Diagnostic Testsmentioning

confidence: 99%

Untitled

2005

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Antineutrophil antibodies are well recognized causes of neutropenia, producing both quantitative and qualitative defects in neutrophils and increased risk for infection. In primary autoimmune neutropenia (AIN) of infancy, a moderate to severe neutropenia is the sole abnormality; it is rarely associated with serious infections and exhibits a self-limited course. Chronic idiopathic neutropenia of adults is characterized by occurrence in late childhood or adulthood, greater prevalence among females than among males, and rare spontaneous remission. Secondary AIN is more commonly seen in adults and underlying causes include collagen disorders, drugs, viruses and lymphoproliferative disorders. In most patients with AIN, antibodies recognize antigens located on the IgG Fc receptor type 3b but other target antigens have been recently identified in secondary AIN. Granulocyte colonystimulating factor is a proven treatment in patients with AIN of all types and is now preferred to other possible therapies.

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Section: Autoimmune Neutropenias: Pathogenesis and Diagnostic Testsmentioning

confidence: 99%

Untitled

2005

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“…Most of the autoantibodies are directed against the FcγIIIb and the leukocyte adhesion molecule CD11b/CD18 (1). Although the direct causal relationship between AIN and ANCA remains unclear, previous reports suggest the possibility of ANCA-related neutropenia via complementmediated cytotoxicity (12) or phagocytosis (13), which may have affected the neutrophil count of our patient.…”

Section: Discussionmentioning

confidence: 76%

Refractory Adult Primary Autoimmune Neutropenia that Responded to Alemtuzumab

et al. 2016

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Primary autoimmune neutropenia (P-AIN) is an extremely rare disease. The most effective treatment for primary P-AIN is a granulocyte colony-stimulating factor; however, no curative treatment has been reported. We herein report a case of an adult P-AIN patient with a relatively mild medical history (irrespective of the severe neutropenia) who showed a sustained hematological response over seventeen months after the initiation of treatment with subcutaneous Alemtuzumab.

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“…Binding of radioiodinated SPA to normal paraformaldehyde-fixed neutrophils (2x107/mL) that had been previously incubated (60 minutes at 37°C) with equal volume of flecanide acetate (either 3.3 mg/mL or 0.33 mg/mL) or buffer and then extensively washed, was assayed as previously described. 13 Significant increase in SPA binding was observed subsequent to incubation of flecanide-exposed neutrophils with patient's serum, indicating specific binding of an IgG antibody. The results are the mean ± SEM of triplicate assays.…”

Section: Resultsmentioning

confidence: 93%

Flecanide-Induced Immune Neutropenia

Samlowski¹

1987

Arch Intern Med

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Activation of human complement by immunoglobulin G antigranulocyte antibody.

Cited by 23 publications

References 33 publications

Untitled

Untitled

Refractory Adult Primary Autoimmune Neutropenia that Responded to Alemtuzumab

Flecanide-Induced Immune Neutropenia

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