| |
|
|
|
|
|
|
|||
|
Blood, 10 September 2009, Vol. 114, No. 11, pp. 2315-2322. Prepublished online as a Blood First Edition Paper on June 12, 2009; DOI 10.1182/blood-2009-04-214387.
Submitted April 2, 2009
Center for Transfusion and Cellular Therapies, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, United States * Corresponding author; email: jzimrin{at}emory.edu.
When successful, HLA matched bone marrow transplantation (BMT) with reduced intensity conditioning is a cure for several non-malignant hematological disorders that require chronic transfusion, such as sickle cell disease and aplastic anemia. However, there are unusually high BMT rejection rates in these patients. Rejection correlates with the number of pre-BMT transfusions, and it has been hypothesized that pre-immunization to antigens on transfused blood may prime BMT rejection. Using a novel mouse model of RBC transfusion and MHC matched BMT, we report that transfusion of RBC products induced BMT rejection across minor histocompatibility antigen (mHA) barriers. It has been proposed that contaminating leukocytes are responsible for transfusion-induced BMT rejection; however, filter leukoreduction did not prevent rejection in the current studies. Moreover, we generated a novel transgenic mouse with RBC specific expression of a model mHA, and demonstrated that transfusion of RBCs induced a CD8+ T cell response. Together, these data suggest that mHAs on RBCs themselves are capable of inducing BMT rejection. Cellular immunization to mHAs is neither monitored nor managed by current transfusion medicine practice; however, the current data suggest that mHAs on RBCs may represent an unappreciated and significant consequence of RBC transfusion.
Related Article in Blood Online:
This article has been cited by other articles:
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Copyright © 2009 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||