Transfusion‐related acute lung injury caused by human leucocyte antigen class II antibody

Flesch, Brigitte K.; Neppert, J.

doi:10.1046/j.0007-1048.2001.03305.x

Cited by 98 publications

(80 citation statements)

References 14 publications

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“…The latter aspect cannot be excluded because a healthy volunteer developed TRALI after infusion of HLA class II antibodies. 20 Plasma that has been used in our experiments were from females with a history of pregnancy, but none of these donors was involved in a TRALI case. It is thus not clear whether they are representative of TRALI.…”

Section: Hla Class II Antibody-inducedmentioning

confidence: 99%

“…A number of case reports were published subsequently, [16][17][18][19] and plasma containing anti-HLA DR was shown to cause TRALI in a healthy male volunteer in an experimental setting. 20 Currently available data from large series and published hemovigilance reports indicate that HLA class II antibodies matching the recipients' antigens are present in ϳ 50% of all TRALI cases and thus represent the most frequently detected matched antibodies in implicated donors. 15,[21][22][23][24][25] HLA class II molecules can be found on alveolar macrophages, which are unlikely to be reached by a transfused antibody before the breakdown of the blood-lung barrier and on some blood leukocytes, including monocytes.…”

mentioning

confidence: 99%

“…48 Second, in an in vivo experiment, HLA class II antibodies caused TRALI in a healthy male volunteer. 20 Finally, it has been reported that monocytopenia occurs in patients with TRALI because of HLA class II antibodies. 20,21 In contrast to previous observations with antineutrophil antibodies, 9,10 where the antibody itself was capable of precipitating TRALI in an ex vivo rodent lung model without any additional stimuli, we were unable to induce TRALI with HLA class II antibodies without preactivation of the rat endothelium by LPS.…”

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confidence: 99%

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Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Sachs

Wasel

Bayat

et al. 2011

Blood

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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated mortality in the United States and other countries. In most TRALI cases, human leukocyte antigen (HLA) class II antibodies are detected in implicated donors. However, the corresponding antigens are not present on the cellular key players in TRALI: neutrophils and endothelium. In this study, we identify monocytes as a primary target in HLA class II-induced TRALI. Monocytes become activated when incubated with matched HLA class II antibodies and are capable of activating neutrophils, which, in turn, can induce disturbance of an endothelial barrier. In an ex vivo rodent model, HLA class II antibody-dependent monocyte activation leads to severe pulmonary edema in a relevant period of time, whenever neutrophils are present and the endothelium is preactivated. Our data suggest that in most TRALI cases, monocytes are cellular key players, because HLA class II antibodies induce TRALI by a reaction cascade initiated by monocyte activation. Furthermore, our data support the previous assumption that TRALI pathogenesis follows a threshold model. Having identified the biologic mechanism of HLA class II antibodyinduced TRALI, strategies to avoid plasma from immunized donors, such as women with a history of pregnancy, appear to be justified preventive measures. (Blood. 2011;117(2):669-677) IntroductionTransfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated death in the United States and other countries. 1 It typically presents within 6 hours after transfusion as a clinical syndrome characterized by acute respiratory distress, hypoxemia, and a bilateral pulmonary edema on chest x-ray. 2 The incidence of TRALI has been estimated as 1/5000 for all blood components, and current mortality rates are in the range of 5%-25%. 3 All blood components have been implicated in TRALI, but those containing large amounts of plasma are mainly responsible. [3][4][5] A recently published literature review states that in 80% of all TRALI cases, white blood cell antibodies can be identified in the implicated blood donor, 6 and most implicated donors have been women with a history of pregnancy. Pregnancy results in alloimmunization against paternal white blood cell antigens in 21%-24% of women, 7,8 with 3 main antibody specificities: human leukocyte antigen (HLA) class I, HLA class II, and human neutrophil antigens (HNAs).The capability of antibodies recognizing either HNA 9-11 or HLA class I 12,13 to precipitate TRALI has been proved in different animal models. It is consensus opinion that neutrophil activation is the key mechanism by which antibodies to HNA and to HLA class I mediate TRALI, 4,14 be it by direct binding to the cognate antigen on the surface of the neutrophil [9][10][11]13 or, in the case of HLA class I antibodies, possibly by binding to HLA class I molecules on pulmonary endothelial cells, which leads to neutrophil trapping by the neutrophils' Fc receptors and subsequent neutrophil activation by receptor...

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Section: Hla Class II Antibody-inducedmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Sachs

Wasel

Bayat

et al. 2011

Blood

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“…These may be antibodies to the human leucocyte antigen (HLA) or to other leucocyte antigens. HLA antibodies may be directed against either HLA class I antigens that are present in all leucocytes or HLA class II antigens found on B lymphocytes and monocytes [7,19,[33][34][35][36][37][38] or infusion of donor leucocytes into a recipient whose antibodies are directed against these donor leucocytes [17,39,40]. Most reactions are caused by antibodies in donor plasma and less than 10% of reactions are caused by plasma antibodies in the recipient that agglutinate the donor leucocytes [17,39,40].…”

Section: The Antibody-mediated Modelmentioning

confidence: 99%

Transfusion‐related acute lung injury: a literature review

Barrett

Kam

2006

Anaesthesia

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SummaryTransfusion-related acute lung injury (TRALI) is a serious and potentially fatal complication of transfusion of blood and blood components. TRALI is under-diagnosed and under-reported because of a lack of awareness. A number of models have been proposed to explain the pathogenesis of TRALI: an antibody mediated model; a two-event biologically active mediator model; and a combined model. TRALI can occur with any type of blood product and can occur with as little as one unit. Its presentation is similar to other forms of acute lung injury and management is predominantly supportive. The main strategy in combating TRALI is prevention both through manipulation of the donor pool and through clinical strategies directed at reducing transfusion of blood products including, but not limited to, evidence-based lower transfusion thresholds.

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“…It is dose-dependent and typically associated with plasma, although low volumes of plasma, such as the quantity within red cell units (2-100 mL), cryoprecipitate, and intravenous immunoglobulin [88] may be sufficient to cause TRALI. A threshold model [86] describes who does, or does not, develop TRALI [88,89].…”

Section: Transfusion-related Acute Lung Injurymentioning

confidence: 99%

Red cell transfusion and the immune system

2014

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SummaryUnderstanding the complex immunological consequences of red cell transfusion is essential if we are to use this valuable resource wisely and safely. The decision to transfuse red cells should be made after serious considerations of the associated risks and benefits. Immunological risks of transfusion include major incompatibility reactions and transfusion-related acute lung injury, while other immunological insults such as transfusion-related immunomodulation are relatively underappreciated. Red cell transfusions should be acknowledged as immunological exposures, with consequences weighed against expected benefits. This article reviews immunological consequences and the emerging evidence that may inform risk-benefit considerations in clinical practice.

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Transfusion‐related acute lung injury caused by human leucocyte antigen class II antibody

Cited by 98 publications

References 14 publications

Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Transfusion‐related acute lung injury: a literature review

Red cell transfusion and the immune system

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