Journal
JOURNAL OF IMMUNOLOGY
Volume 177, Issue 11, Pages 7715-7722Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.11.7715
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Funding
- NIDDK NIH HHS [DK 049814, DK 064603] Funding Source: Medline
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Acute allograft rejection requires the activation of alloreactive CD4 T cells. Despite the capacity of B cells to act as potent APCs capable of activating CD4 T cells in vivo, their role in the progression of acute allograft rejection was unclear. To determine the contribution of B cell APC function in alloimmunity, we engineered mice with a targeted deficiency of MHC class II-mediated Ag presentation confined to the B cell compartment. Cardiac allograft survival was markedly prolonged in these mice as compared to control counterparts (median survival time, > 70 vs 9.5 days). Mechanistically, deficient B cell-mediated Ag presentation disrupted both alloantibody production and the progression of CD4 T cell activation following heart transplantation. These findings demonstrate that indirect alloantigen presentation by recipients' B cells plays an important role in the efficient progression of acute vascularized allograft rejection.
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