MHC class I-specific antibody binding to nonhematopoietic cells drives complement activation to induce transfusion-related acute lung injury in mice
| Autor: | Nathaniel Barasa, Richard T. Strait, Nico van Rooijen, Wyenona Hicks, Marat Khodoun, Ashley Mahler, B. M. Susskind, David P. Witte, Jörg Köhl, Keith F. Stringer, Fred D. Finkelman |
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| Přispěvatelé: | Molecular cell biology and Immunology, CCA - Immuno-pathogenesis |
| Rok vydání: | 2011 |
| Předmět: |
Genotype
Acute Lung Injury Immunology Enzyme-Linked Immunosorbent Assay Lung injury Major histocompatibility complex Bronchoalveolar Lavage Polymerase Chain Reaction Article Pathogenesis Mice Microscopy Electron Transmission MHC class I medicine Animals Immunology and Allergy Complement Activation DNA Primers Mice Inbred BALB C biology Macrophages H-2 Antigens Antibodies Monoclonal Transfusion Reaction respiratory system medicine.disease Pulmonary edema Mice Mutant Strains Complement system Microscopy Fluorescence Blood Group Incompatibility biology.protein Regression Analysis Antibody Reactive Oxygen Species Transfusion-related acute lung injury |
| Zdroj: | Strait, R T, Hicks, W, Barasa, N, Mahler, A, Khodoun, M, Kohl, J, Stringer, K, Witte, D, van Rooijen, N, Susskind, B M & Finkelman, F D 2011, ' MHC class I-specific antibody binding to nonhematopoietic cells drives complement activation to induce transfusion-related acute lung injury in mice ', Journal of Experimental Medicine, vol. 208, no. 12, pp. 2525-2544 . https://doi.org/10.1084/jem.20110159 Journal of Experimental Medicine, 208(12), 2525-2544. Rockefeller University Press The Journal of Experimental Medicine |
| ISSN: | 0022-1007 |
| DOI: | 10.1084/jem.20110159 |
| Popis: | In a manner partially independent of activating Fcγ receptors, antibody-mediated production of complement component C5a and recruitment of macrophages elicit transfusion-related acute lung injury in mice. Transfusion-related acute lung injury (TRALI), a form of noncardiogenic pulmonary edema that develops during or within 6 h after a blood transfusion, is the most frequent cause of transfusion-associated death in the United States. Because development of TRALI is associated with donor antibodies (Abs) reactive with recipient major histocompatibility complex (MHC), a mouse model has been studied in which TRALI-like disease is caused by injecting mice with anti–MHC class I monoclonal Ab (mAb). Previous publications with this model have concluded that disease is caused by FcR-dependent activation of neutrophils and platelets, with production of reactive oxygen species that damage pulmonary vascular endothelium. In this study, we confirm the role of reactive oxygen species in the pathogenesis of this mouse model of TRALI and show ultrastructural evidence of pulmonary vascular injury within 5 min of anti–MHC class I mAb injection. However, we demonstrate that disease induction in this model involves macrophages rather than neutrophils or platelets, activation of complement and production of C5a rather than activation of FcγRI, FcγRIII, or FcγRIV, and binding of anti–MHC class I mAb to non-BM–derived cells such as pulmonary vascular endothelium. These observations have important implications for the prevention and treatment of TRALI. |
| Databáze: | OpenAIRE |
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