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Blood, Vol. 109, Issue 11, 5049-5057, June 1, 2007
Effector and regulatory T-cell function is differentially regulated by RelB within antigen-presenting cells during GVHD
Blood MacDonald et al.
109: 5049
Supplemental materials for: MacDonald et al, Vol 109, Issue 11, 5049-5057
Files in this Data Supplement:
- Figure S1. BMC Treg numbers and DC phenotype after transplantation (PDF, 66.4 KB) -
(A) Attenuation of GVHD in RelB/ BMC in the Balb/c → B6 model is a CD4-dependent process. WT and RelB/ BMCs were transplanted with allogeneic (n = 7 per group) or syngeneic (n = 3) BM and 1.5 × 106 purified CD4+ T cells. *P < .05. (B) Treg development in RelB/ and WT BMCs. Absolute number and percentage of CD4+FoxP3+ T cells within total CD4+ population in the spleen of WT (n = 10) and RelB/ (n = 9) BMCs, ***P < .001. Absolute numbers are NS. (C) Costimulatory molecule expression on reconstituting donor DCs after BMT. B6D2F1 recipients received transplants of WT or RelB/ BM with RelB-replete T cells, and reconstituting CD11chi DCs within the spleen were phenotyped 14 days later. Red line indicates RelB/ DCs; blue line, WT DCs; black line, TCDs; thin black line, isotype control.
- Figure S2. Donor CD4 T cells from RelB/ BMCs produce large amounts of Th2 cytokines (PDF, 243 KB) -
(A) Donor splenic CD4+ T cells were sort-purified from allogeneic BMC transplant recipients 10 days after BMT and restimulated in culture by plate-bound Abs to CD3 and CD28 (both at 10 µg/mL) or alloantigen (B6D2F1 DCs). IFN , IL-4, and IL-5 production from donor CD4+ T cells in response to Abs (B) and alloantigen (B) were determined in culture supernatants as described in “Materials and methods.” Results represent mean ± SEM of triplicate wells. Data are from 1 of 3 representative experiments. (C) The absence of RelB within donor APCs does not inhibit GVL. Xenogen biophotonic imaging of leukemia development in irraditated B6D2F1 recipients that received transplants of WT or RelB/ BM with (+T, n = 12/group) or without (TCD, n = 4/group) purified RelB-replete T cells followed by the transfer of 5 × 104 host-type P815 transfected with a luciferase reporter gene 14 days after BMT, when donor APCs had reconstituted. Recipients of WT and RelB/ TCD BM developed leukemia by day 28 (shown), and all died within 36 days of BMT, whereas leukemia was eliminated in recipients of both WT or RelB/ T-cellreplete grafts with no leukemia evident in either recipient group 50 days after BMT.
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