Figure 3.
Figure 3. In vivo chimerism level and anti-αGal Ab levels over time. (A) αGal expression assessed by flow cytometry as lectin-IB4 binding cells in various cell lineages in the peripheral blood of GalT-transduced BMT mice (n = 5). Whole PBCs (Total), T cells (CD3), B cells (CD19), granulocytes (Ly6G/C), erythroid lineage cells (TeR119). Data are shown as mean ± SE. (B) Genomic integration of GalT was assessed by quantitative PCR. Lentiviral vector–specific forward primer and porcine GalT–specific reverse primers were used for quantitative genomic PCR (n = 5 each). Data are shown as mean ± SE. KO indicates knockout. (C) Anti-αGal Ab levels were assessed by ELISA in GalT BMT (□), REV BMT (•), IR controls (▴) (n = 5 each). Xenoantibodies that bind to αGal are not produced in GalT BMT mice. Data are shown as mean ± SE.

In vivo chimerism level and anti-αGal Ab levels over time. (A) αGal expression assessed by flow cytometry as lectin-IB4 binding cells in various cell lineages in the peripheral blood of GalT-transduced BMT mice (n = 5). Whole PBCs (Total), T cells (CD3), B cells (CD19), granulocytes (Ly6G/C), erythroid lineage cells (TeR119). Data are shown as mean ± SE. (B) Genomic integration of GalT was assessed by quantitative PCR. Lentiviral vector–specific forward primer and porcine GalT–specific reverse primers were used for quantitative genomic PCR (n = 5 each). Data are shown as mean ± SE. KO indicates knockout. (C) Anti-αGal Ab levels were assessed by ELISA in GalT BMT (□), REV BMT (•), IR controls (▴) (n = 5 each). Xenoantibodies that bind to αGal are not produced in GalT BMT mice. Data are shown as mean ± SE.

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