Transfusion‐related acute lung injury due to HLA‐A2‐specific antibodies in recipient and NB1‐specific antibodies in donor blood

Bux, Jürgen; Becker, Frank; Seeger, Werner; Kilpatrick, David C.; Chapman, J. F.; Waters, A. H.

doi:10.1046/j.1365-2141.1996.d01-1703.x

Cited by 173 publications

(147 citation statements)

References 15 publications

(23 reference statements)

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“…Serological work up of TRALI patients identified antibodies to a HNA in a number of cases (Yomtovian et al, 1984;Nordhagen et al, 1986;Bux et al, 1996;Leach et al, 1998); a description of HNA antigens and their implication in TRALI has been published previously (Bux, 2005).…”

Section: Antibodies To Human Neutrophil Antigensmentioning

confidence: 99%

The pathogenesis of transfusion‐related acute lung injury (TRALI)

2007

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SummaryIn recent years, transfusion-related acute lung injury (TRALI) has developed from an almost unknown transfusion reaction to the most common cause of transfusion-related major morbidities and fatalities. A clinical definition of TRALI was established in 2004, based on acute respiratory distress, noncardiogenic lung oedema temporal association with transfusion and hypoxaemia. Histological findings reveal lung oedema, capillary leucostasis and neutrophil extravasation. However, the pathogenesis of TRALI remains controversial. Leucocyte antibodies, present in fresh frozen plasma and platelet concentrates from multiparous donors, and neutrophil priming agents released in stored cellular blood components have been considered to be causative. As neutrophils and endothelial cells are pivotal in the pathogenesis of TRALI, a threshold model was established to try to unify the various reported findings on pathogenesis. This model comprises the priming of neutrophils and/or endothelium by the patient's co-morbidity, neutrophil and/or endothelial cell activation by the transfused blood component, and the severity of the TRALI reaction.

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Section: Antibodies To Human Neutrophil Antigensmentioning

confidence: 99%

The pathogenesis of transfusion‐related acute lung injury (TRALI)

2007

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“…6,15 In a small percent of cases, the leukoagglutinating antibody appears to be from the recipient and is directed at the transfused neutrophils. [16][17][18] Most of the donors implicated in TRALI have been multiparous women who became alloimmunized during pregnancy. The frequency of sensitization to HLA class I and class II correlates with parity, with 2-8%, 10-15%, and 17-26% identified in women with zero, 1-2, or ≥ 3 pregnancies, respectively.…”

Section: Immune (Antibody)-mediated Tralimentioning

confidence: 99%

Transfusion-Related Acute Lung Injury: An Update

Triulzi

2006

Hematology

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Transfusion-associated acute lung injury (TRALI) has emerged as a leading cause of transfusion-related morbidity and mortality. TRALI is characterized by acute non-cardiogenic pulmonary edema and respiratory compromise in the setting of transfusion. The study of TRALI has been hampered by inadequate case definitions and an incomplete understanding of the pathologic mechanisms. Recent consensus conferences took an important first step by providing a framework for case definition. Recent advances in the understanding of the pathogenesis of TRALI have also occurred. TRALI has been primarily attributed to donor leukocyte antibodies that are thought to interact with recipient neutrophils, resulting in activation and aggregation in pulmonary capillaries, release of local biologic response modifiers causing capillary leak, and lung injury. An alternate mechanism termed the "two hit" or "neutrophil priming" hypothesis postulates that a pathway to neutrophil activation and aggregation can occur without leukocyte antibodies. A first event such as sepsis or trauma can induce pulmonary endothelial activation, release of cytokines, and priming of neutrophils. A subsequent second event such as exposure to lipids, cytokines or antibodies in a blood component would then cause activation of adherent neutrophils and a release of bioreactive molecules leading to lung injury. There are limited clinical and animal studies to support the "two hit" model. These proposed mechanisms are not mutually exclusive in that donor leukocyte antibody can be pathogenic in both models and have implications for new strategies to prevent TRALI.Advances in blood safety have greatly reduced the risk of transfusion-associated infectious disease transmission. As a result, noninfectious serious hazards of transfusion have come to the forefront as increasingly important blood safety issues. Transfusion-associated acute lung injury (TRALI) has emerged as a leading cause of transfusion related morbidity and mortality.1 This report will summarize recent consensus conferences that have provided practical clinical definitions of TRALI to aid the clinician in diagnosis and to facilitate its study. Recent advances in understanding of the pathogenesis of TRALI will be presented with a potential unifying hypothesis. DefinitionA lack of a standardized definition of TRALI has hindered accurate clinical diagnosis, epidemiology, and research investigation. A recent NHLBI working group convened to identify research needs addressed this critical issue by providing the following definition: "new acute lung injury (ALI) occurring during or within 6 hours after a transfusion, with a clear temporal relationship to transfusion, in patients without or with risk factors for ALI other than transfusion."2 Limitations to the proposed NHLBI working group definition are the exclusion of patients with preexisting ALI, excluding cases with onset more than 6 hours after transfusion, lack of laboratory diagnostic criteria, and a required severity of hypoxia that would miss cases of mil...

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“…NB1 alloimmunization is clinically important because NB1 alloantibodies can cause immune neutropenia and transfusion-related acute lung injury. 1,[14][15][16][17][18][19] …”

Section: Introductionmentioning

confidence: 99%

Molecular basis of NB1 (HNA-2a, CD177) deficiency

Kissel

Scheffler

Kerowgan

et al. 2002

Blood

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Alloimmunization to the neutrophil antigen NB1 (HNA-2a, CD177) can result in immune neutropenia and transfusionrelated acute lung injury. Recently, we were able to elucidate the primary structure of NB1. To shed light also on the molecular basis of the NB1-negative phenotype, we studied the neutrophils of 2 women with NB1-specific alloantibodies for intracellular and extracellular NB1 expression, NB1-specific mRNA production, and the presence of the NB1 gene. No antibody binding to neutrophils was observed by immunofluorescence and immunoblot using a variety of human and monoclonal NB1-specific antibodies. By reverse transcription-polymerase chain reaction with NB1-specific primers we could not detect NB1 cDNAs without accessory sequences, which were found to be introns. The NB1 gene was present in the genome of both patients. Our data indicate that the NB1-negative phenotype is the result of different off-frame insertions on RNA level, resulting in NB1 deficiency on neutrophils. (Blood. 2002;99: 4231-4233)

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Transfusion‐related acute lung injury due to HLA‐A2‐specific antibodies in recipient and NB1‐specific antibodies in donor blood

Cited by 173 publications

References 15 publications

The pathogenesis of transfusion‐related acute lung injury (TRALI)

The pathogenesis of transfusion‐related acute lung injury (TRALI)

Transfusion-Related Acute Lung Injury: An Update

Molecular basis of NB1 (HNA-2a, CD177) deficiency

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