T-cell suppression by red blood cells is dependent on intact cells and is a consequence of blood bank processing
Article first published online: 4 NOV 2013
© 2013 American Association of Blood Banks
Volume 54, Issue 5, pages 1340–1347, May 2014
How to Cite
Long, K., Meier, C., Bernard, A., Williams, D., Davenport, D. and Woodward, J. (2014), T-cell suppression by red blood cells is dependent on intact cells and is a consequence of blood bank processing. Transfusion, 54: 1340–1347. doi: 10.1111/trf.12472
- Issue published online: 12 MAY 2014
- Article first published online: 4 NOV 2013
- Manuscript Accepted: 14 SEP 2013
- Manuscript Revised: 15 AUG 2013
- Manuscript Received: 12 JUN 2013
- National Center for Advancing Translational Sciences. Grant Number: UL1TR000117
- Dean of the College of Medicine, University of Kentucky
Red blood cells (RBCs) suppress T-cell responsiveness through a mechanism requiring cell–cell contact. Questions remain as to whether this effect is an allogeneic response, related to cell death, or dependent on particular components of the RBCs.
Study Design and Methods
Peripheral T cells were isolated from healthy donors and exposed to stored allogeneic RBCs or autologous RBCs after processing. RBCs were lysed by hypotonic solvent to produce cellular ghosts. Tritiated thymidine proliferation assays were utilized. Cultures were saturated with interleukin (IL)-2 to determine whether impaired IL-2 synthesis played a role.
T-cell proliferation was suppressed by both autologous and allogeneic RBCs. RBC membrane integrity does enhance T-cell suppression. T-cell death is not responsible for the suppressive changes. IL-2 synthesis is suppressed in RBC-exposed T cells but addition of exogenous IL-2 does not rescue proliferative capabilities. Proliferation of T cells was inhibited with RBC exposure but mitigated with the addition of fresh RBCs.
T-cell suppression is enhanced by intact RBCs but this effect is unrelated solely to alloantigens. Neither apoptosis nor necrosis of T cells contributes to this phenomenon. IL-2 synthesis is suppressed after RBC exposure as a consequence of T-cell inhibition, but is not the primary cause of suppression. Fresh RBCs do not mediate T-cell suppression, indicating that changes in the RBC and development of the storage lesion may occur during initial blood bank processing.