An association of soluble CD40 ligand (CD154) with adverse reactions to platelet transfusions

Blumberg, Neil; Gettings, Kelly F.; Turner, Chantal; Heal, Joanna M.; Phipps, Richard P.

doi:10.1111/j.1537-2995.2006.00979.x

Cited by 136 publications

(131 citation statements)

References 27 publications

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“…When PLTs are stored for a long period of time, they release soluble CD154 (31) and can shed MHC (32). In addition, during storage, residual leukocytes and/or PLTs in the PRP concentrates can release various proinflammatory mediators (31,33,34). In theory, these storage-based changes may alter the immune responses to transfused PLTs.…”

Section: Discussionmentioning

confidence: 99%

Transfusion of minor histocompatibility antigen–mismatched platelets induces rejection of bone marrow transplants in mice

Patel

Cadwell²,

Medford³

et al. 2009

J. Clin. Invest.

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Bone marrow transplantation (BMT) represents a cure for nonmalignant hematological disorders. However, compared with the stringent conditioning regimens used when performing BMT to treat hematological malignancies, the reduced intensity conditioning regimen used in the context of nonmalignant hematological disorders leads to substantially higher rates of BMT rejection, presumably due to an intact immune system. The relevant patient population typically receives transfusion support, often including platelets, and the frequency of BMT rejection correlates with the frequency of transfusion. Here, we demonstrate that immunity to transfused platelets contributes to subsequent BMT rejection in mice, even when the BMT donor and recipient are MHC matched. We used MHC-matched bone marrow because, although immunity to transfused platelets is best characterized in relation to HLA-specific antibodies, such antibodies are unlikely to play a role in clinical BMT rejection that is HLA matched. However, bone marrow is not matched in the clinic for minor histocompatibility antigens, such as those carried by platelets, and we report that transfusion of minor histocompatibility antigen-mismatched platelets induced subsequent BMT rejection. These findings indicate previously unappreciated sequelae of immunity to platelets in the context of transplantation and suggest that strategies to account for minor histocompatibility mismatching may help to reduce the chance of BMT rejection in human patients.

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Section: Discussionmentioning

confidence: 99%

Transfusion of minor histocompatibility antigen–mismatched platelets induces rejection of bone marrow transplants in mice

Patel

Cadwell²,

Medford³

et al. 2009

J. Clin. Invest.

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show abstract

“…93,94 Data regarding the role of altered protein C and S, factor VIII and von Willebrand factor levels secondary to EPO administration are inconsistent, 95 and proposed novel mechanisms point to increased creactive protein activity, nitric oxide and thrombinactivatable fibrinolysis inhibitor (TAFI) as the causative factors for EPOrelated thrombosis. 96 Blood and blood component transfusion Khorana et 3 Possible mechanisms of transfusioninduced thrombosis include inadvertent delivery of prothrombotic mediators such as activated platelets, platelet microparticles and sCD40L; 97,98 increased circulating RBC mass and consequent vascular stasis; vasoconstriction due to nitric oxidedepleted RBCs; 99 and delivery of increased redoxactive iron, resulting in oxidative stress.…”

Section: Supportive Therapies Related To Arterial Thromboembolism Erymentioning

confidence: 99%

Peripheral arterial ischemic events in cancer patients

2010

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Thromboembolic complications are the second leading cause of death in cancer patients. In contrast to the large body of literature on venous thromboembolism (VTE), relatively few reports have focused on the pathogenesis, incidence, management and outcomes of arterial thromboembolic events in patients with malignancy. The purpose of this article is to review the current literature on the etiology, mechanisms, and prognosis of arterial thromboembolic events in cancer patients and outline appropriate screening and management guidelines that may help lower the rates of morbidity and mortality related to these events.

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“…Potential NAFs that accumulate during the routine storage of blood products include lyso-phosphatidylcholines (lysoPCs) [9,36,[38][39][40][41], neutral lipids [34,[38][39][40][41], sCD40L [42][43][44][45], cytokines [37,45,46] and microparticles (MPs) [47,48]. Some NAFs have the ability to prime for PMN respiratory burst [9,34,36,[38][39][40]43].…”

Section: Non-antibody Factors (Nafs)mentioning

confidence: 99%

Evidence behind the pathophysiology of TRALI

Tung

Minchinton

Fraser

et al. 2011

ISBT Science Series

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Transfusion-related acute lung injury (TRALI) is a serious transfusion complication that may lead to significant morbidity and mortality. This has driven a significant research effort focused on understanding why and how TRALI develops. The ultimate goal must be prevention or at least mitigation of the clinical consequences of TRALI.The underlying pathophysiology of TRALI is presently best described by two hypotheses which are not mutually exclusive. These are the antibody mediated TRALI mechanism and the two-event or priming TRALI mechanism. One of the key initial findings in TRALI research was the frequent presence of leucocyte antibodies in associated blood products, providing strong evidence for an antibody driven pathogenesis. In contrast, the two-event mechanism proposed that these transfused antibodies activated neutrophils that had first been primed by the patient's clinical condition.Together, data from haemovigilance programs, clinical reports and experimental findings have led several countries to introduce TRALI risk-reduction strategies. These include either limiting the transfusion of plasma from female donors or, screening female donors for the presence of leucocyte antibodies. Both approaches are justified by adoption of the immune mechanism as the prime driver of the pathogenesis of TRALI. TRALI incidence has gratifyingly been reduced by these measures. Nevertheless, TRALI cases persist and they remain a major concern because of continuing significant morbidity and mortality.While the majority of earlier TRALI research has focused on the role of antibodies in TRALI, evidence for the role of non-antibody factors in TRALI is now growing, based on an increasing number of in vitro, ex vivo and in vivo models. This review aims to present data from such models, which are the foundation for our current understanding of the pathophysiology behind antibody mediated and non-antibody mediated TRALI.

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An association of soluble CD40 ligand (CD154) with adverse reactions to platelet transfusions

Abstract: These are the first data demonstrating that a PLT-derived mediator, sCD40L, is associated with adverse transfusion events. Existing clinical factors, for example, inflammation or leukopenia, may influence whether infused mediators cause reactions.

Cited by 136 publications

References 27 publications

Transfusion of minor histocompatibility antigen–mismatched platelets induces rejection of bone marrow transplants in mice

Transfusion of minor histocompatibility antigen–mismatched platelets induces rejection of bone marrow transplants in mice

Peripheral arterial ischemic events in cancer patients

Evidence behind the pathophysiology of TRALI

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