Targeting Cells Causing Split Tolerance Allows Fully Allogeneic Islet Survival With Minimal Conditioning in NOD Mixed Chimeras
Article first published online: 13 SEP 2012
© Copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons
American Journal of Transplantation
Volume 12, Issue 12, pages 3235–3245, December 2012
How to Cite
Al-Adra, D. P., Pawlick, R., Shapiro, A. M. J. and Anderson, C. C. (2012), Targeting Cells Causing Split Tolerance Allows Fully Allogeneic Islet Survival With Minimal Conditioning in NOD Mixed Chimeras. American Journal of Transplantation, 12: 3235–3245. doi: 10.1111/j.1600-6143.2012.04260.x
- Issue published online: 30 NOV 2012
- Article first published online: 13 SEP 2012
- Received 28 June 2012, revised 19 July 2012 and accepted for publication 06 August 2012
Figure S1: Characterization of NOD.GFP→B6.g7 and B6.g7→NOD.GFP radiation chimeras. (A) Diabetes incidence of NOD.wt, NOD.GFP and radiation chimeras. (B) After 5 weeks, to allow for hematopoietic cell reconstitution, peripheral blood of full chimeras was assessed by flow cytometry. Full chimerism was assessed in NOD.GFP→B6.g7 and B6.g7→NOD.GFP mice by gating on peripheral blood live cells and determining the expression of GFP. Lymphocytes of reconstituted B6.g7 mice were 94.0 ± 1.0% NOD.GFP in origin, and reconstituted NOD.GFP mice were 96.3 ± 0.6% B6.g7 in origin. (C) Donor lymphocyte gated T and B cell frequency in peripheral blood at 5 weeks postradiation and BMT.
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