期刊
CELL REPORTS
卷 15, 期 6, 页码 1214-1227出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.04.009
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资金
- British Heart Foundation project grant
- National Institute of Health Research (NIHR) Cambridge Biomedical Research Centre
- NIHR Blood and Transplant Research Unit in Organ Donation and Transplantation at the University of Cambridge
- NHS Blood and Transplant (NHSBT)
- Wellcome Trust Clinical Research Training Fellowships
- Raymond Scholarship
- Beverly Sackler Scholarship
- Addenbrooke's Charitable Trust Clinical Research Fellowship
Chronic rejection of solid organ allografts remains the major cause of transplant failure. Donor-derived tissue-resident lymphocytes are transferred to the recipient during transplantation, but their impact on alloimmunity is unknown. Using mouse cardiac transplant models, we show that graft-versus-host recognition by passenger donor CD4 T cells markedly augments recipient cellular and humoral alloimmunity, resulting in more severe allograft vasculopathy and early graft failure. This augmentation is enhanced when donors were pre-sensitized to the recipient, is dependent upon avoidance of host NK cell recognition, and is partly due to provision of cognate help for allo-specific B cells from donor CD4 T cells recognizing B cell MHC class II in a peptide-degenerate manner. Passenger donor lymphocytes may therefore influence recipient alloimmune responses and represent a therapeutic target in solid organ transplantation.
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