Prevalence of granulocyte antibodies in never allo-exposed female and male donors

2016 ◽  
Vol 98 (3) ◽  
pp. 250-253 ◽  
Author(s):  
Rutger A. Middelburg ◽  
Hans Vrielink ◽  
Leendert Porcelijn
Keyword(s):  
Granulocyte Antibodies

A Comparison of Immunofluorescent Assays to Detect Anti-Granulocyte Antibodies

1985 ◽  
Vol 84 (4) ◽  
pp. 464-468 ◽  
Author(s):  
Mary L. Lape ◽  
James A. Baker ◽  
John K. Chan
Keyword(s):  
Granulocyte Antibodies

Detection of granulocyte antibodies using simultaneous analysis of specific granulocyte antibodies assay (SASGA)

Vox Sanguinis ◽  
2011 ◽  
Vol 101 (2) ◽  
pp. 147-153 ◽  
Author(s):  
X. D. Nguyen ◽  
R. Scherpf ◽  
F. Sassenhof ◽  
B. Flesch ◽  
H. Klüter
Keyword(s):  
Simultaneous Analysis ◽  
Granulocyte Antibodies

scholarly journals Are Antineutrophil Antibodies (Granulocyte Antibodies) in Children with HIV Infection Causally Related to Neutropenia? ♦ 783

1997 ◽  
Vol 41 ◽  
pp. 133-133
Author(s):  
Geoffrey A. Weinberg ◽  
David N. Korones ◽  
David F. Stroncek ◽  
Gail Eiber ◽  
Barbara Kassman ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Granulocyte Antibodies

Transfusion-Related Acute Lung Injury Secondary to Biologically Active Mediators

2001 ◽  
Vol 125 (4) ◽  
pp. 523-526
Author(s):  
Susan E. Lenahan ◽  
Ronald E. Domen ◽  
Christopher C. Silliman ◽  
Charles P. Kingsley ◽  
Paula J. Romano
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Distress Syndrome ◽  
Biologically Active ◽  
Blood Components ◽  
Hla Antibodies ◽  
Granulocyte Antibodies ◽  
Priming Activity ◽  
Stored Blood

Abstract Transfusion-related acute lung injury is seen following the transfusion of blood components. The reported incidence is approximately 1 in 2000 transfusions. Clinically, it is similar to adult respiratory distress syndrome. The pathophysiology is unclear but has been attributed to HLA antibodies, granulocyte antibodies, and more recently to biologically active mediators in stored blood components. We report a case with laboratory evidence that supports the role of biologically active mediators in the pathogenesis of transfusion-related acute lung injury. To our knowledge, the case reported here is the first to use lipid extractions of patient samples to determine that lipid-priming activity was present at the time transfusion-related acute lung injury was identified clinically.

Granulocyte antibodies in leukaemic chronic lymphoproliferative disorders

1987 ◽  
Vol 66 (4) ◽  
pp. 461-465 ◽  
Author(s):  
Pradip K. Rustagi ◽  
Tin Han ◽  
Lynn Ziolkowski ◽  
Deborah L. Farolino ◽  
Mark S. Currie ◽  
...  
Keyword(s):  
Lymphoproliferative Disorders ◽  
Granulocyte Antibodies

Serological, Immunochemical and Immuoncytological Properties of Granulocyte Antibodies

Vox Sanguinis ◽  
1978 ◽  
Vol 35 (5) ◽  
pp. 294-303 ◽  
Author(s):  
F.W.A. Verheugt ◽  
A.E.G.K. von dem Borne ◽  
J.C. van Noord-Bokhorst ◽  
E.H. van Elven ◽  
C.P. Engelfriet
Keyword(s):  
Granulocyte Antibodies

Ivig, but Not a Monoclonal Anti-RBC Antibody, Requires the Presence of Gr-1+ Cells to Ameliorate Immune Thrombocytopenia in a Murine Model

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 268-268
Author(s):  
Andrew R. Crow ◽  
Alan H Lazarus
Keyword(s):  
Murine Model ◽  
Conflicts Of Interest ◽  
Ivig Therapy ◽  
Cell Types ◽  
Suppressive Effect ◽  
Cell Depletion ◽  
Peripheral Blood Neutrophil ◽  
Intermediary Cell ◽  
Granulocyte Antibodies ◽  
Dependent Pathway

Abstract Abstract 268 Although there are many theories as to the mechanism of action of IVIg in the treatment of autoimmune disease, the exact pathway by which IVIg functions remains unclear. Many cell populations have been implicated in the IVIg pathway, including dendritic cells, which are considered to be one of the central initiators of IVIg effects, and macrophages, which are involved in platelet destruction. In addition, there is evidence from several groups that additional intermediary cell types may be involved. IVIg administration can induce a suppressive effect on peripheral blood neutrophil counts in ITP patients. In fact, alloimmunized thrombocytopenic patients, who display low neutrophil counts, do not respond to IVIg therapy. Here, we questioned whether Gr-1+cells (consisting primarily of neutrophils) are a critical cell type required for IVIg function, in a murine model of ITP. Another IVIg product which has ameliorative effects similar to IVIg but appears to function via a different mechanism is anti-D. We have previously shown that IVIg and a monoclonal antibody with “anti-D like” activity, TER-119, can successfully ameliorate thrombocytopenia in a murine model of ITP. In human patients as well as murine models of ITP, these 2 therapeutics appear to function via different mechanisms. Some work has shown that IVIg and anti-D work by the same, or overlapping mechanism, while other work shows a notable difference in that IVIg can cause neutropenia under conditions where it works to ameliorate autoimmune inflammation. Mice pretreated with 50 mg IVIg (∼2g/kg), or 50 ug TER-119 thirty min prior to administration of anti-platelet antibody MWReg30, show protection from thrombocytopenia compared with untreated mice. To assess the potential role for Gr-1+ cells in IVIg vs TER-119 mediated amelioration of murine ITP, we used RB6-8C5, a well described rat antibody for Gr-1+ cell depletion. Mice were injected with RB6-8C5 or control rat IgG 24 hr prior to thrombocytopenia induction. Mice pretreated with RB6-8C5 failed to respond to IVIg therapy compared with control mice. In contrast, Gr-1+ cell depletion had no effect on the ability of TER-119 to ameliorate the thrombocytopenia. This suggests that Gr-1+ cells likely play an essential role in IVIg function. In contrast, TER-119, does not depend on the presence of Gr-1+cells, suggesting that the mechanisms of action for IVIg and RBC specific antibodies are different for this requirement. In line with these observations, it has been observed that IVIg can modulate neutrophil activity, suggesting that in the murine ITP model, IVIg may function through a neutrophil dependent pathway. Experiments using more specific granulocyte antibodies will help ascertain whether neutrophils or some other Gr-1+ cell population is involved in IVIg function. Disclosures: No relevant conflicts of interest to declare.

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