Journal
BLOOD
Volume 129, Issue 18, Pages 2557-2569Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2016-12-758185
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Funding
- Health Canada
- Canadian Blood Services
- National Institutes of Health (NIH)
- Swiss National Science Foundation [P300PB-164760]
- NIH, National Heart, Lung, and Blood Institute [HL112311, HL126547]
- NIH, National Institute on Aging [AG048022]
- Swiss National Science Foundation (SNF) [P300PB_164760] Funding Source: Swiss National Science Foundation (SNF)
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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related fatalities and is characterized by acute respiratory distress following blood transfusion. Donor antibodies are frequently involved; however, the pathogenesis and protective mechanisms in the recipient are poorly understood, and specific therapies are lacking. Using newly developed murine TRALI models based on injection of anti-major histocompatibility complex class I antibodies, we found CD4(+)CD25(+)FoxP3(+) T regulatory cells (Tregs) and CD11c(+) dendritic cells (DCs) to be critical effectors that protect against TRALI. Treg or DC depletion in vivo resulted in aggravated antibody-mediated acute lung injury within 90 minutes with 60% mortality upon DC depletion. In addition, resistance to antibody-mediated TRALI was associated with increased interleukin-10 (IL-10) levels, and IL-10 levels were found to be decreased in mice suffering from TRALI. Importantly, IL-10 injection completely prevented and rescued the development of TRALI in mice and may prove to be a promising new therapeutic approach for alleviating lung injury in this serious complication of transfusion.
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