title: Recipient T lymphocytes modulate the severity of antibody-mediated transfusion-related acute lung injury.
abstract: Transfusion-related acute lung injury (TRALI) is a serious complication of transfusion and has been ranked as one of the leading causes of transfusion-related fatalities. Nonetheless, many details of the immunopathogenesis of TRALI, particularly with respect to recipient factors are unknown. We used a murine model of antibody-mediated TRALI in an attempt to understand the role that recipient lymphocytes might play in TRALI reactions. Intravenous injection of an IgG2a antimurine major histocompatibility complex class I antibody (34-1-2s) into BALB/c mice induced moderate hypothermia and pulmonary granulocyte accumulation but no pulmonary edema nor mortality. In contrast, 34-1-2s injections into mice with severe combined immunodeficiency caused severe hypothermia, severe pulmonary edema, and approximately 40% mortality indicating a critical role for T and B lymphocytes in suppressing TRALI reactions. Adoptive transfer of purified CD8(+) T lymphocytes or CD4(+) T cells but not CD19(+) B cells into the severe combined immunodeficiency mice alleviated the antibody-induced hypothermia, lung damage, and mortality, suggesting that T lymphocytes were responsible for the protective effect. Taken together, these results suggest that recipient T lymphocytes play a significant role in suppressing antibody-mediated TRALI reactions. They identify a potentially new recipient mechanism that controls the severity of TRALI reactions.
authors.affiliation: Prince Charles Hospital, University of Queensland, Brisbane, Australia.
authors.forename: Yoke Lin
authors.initials: YL
authors.lastname: Fung
authors.forename: Michael
authors.initials: M
authors.lastname: Kim
authors.forename: Arata
authors.initials: A
authors.lastname: Tabuchi
authors.forename: Rukhsana
authors.initials: R
authors.lastname: Aslam
authors.forename: Edwin R
authors.initials: ER
authors.lastname: Speck
authors.forename: Leola
authors.initials: L
authors.lastname: Chow
authors.forename: Wolfgang M
authors.initials: WM
authors.lastname: Kuebler
authors.forename: John
authors.initials: J
authors.lastname: Freedman
authors.forename: John W
authors.initials: JW
authors.lastname: Semple
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology* / Q000276:immunology*; D000818:Animals; D000906:Antibodies / Q000009:adverse effects* / Q000276:immunology; D054426:Chemokine CXCL2 / Q000097:blood / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D007035:Hypothermia / Q000209:etiology / Q000276:immunology; D007074:Immunoglobulin G / Q000009:adverse effects / Q000276:immunology; D008168:Lung / Q000166:cytology / Q000473:pathology; D017710:Lymphocyte Transfusion; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D009504:Neutrophils / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D065227:Transfusion Reaction
chemical_list: D000906:Antibodies; D054426:Chemokine CXCL2; C404915:Cxcl2 protein, mouse; D015395:Histocompatibility Antigens Class I; D007074:Immunoglobulin G