Extended Data Fig. 1: Donor chimerism and CCR5 genotype and phenotype in PBMC after HSCT.
a, The donor chimerism after HSCT was genotypically assessed from a set of 13 genes. Full (100%) donor chimerism was first achieved 34 days after HSCT then dropped to 72% during the second relapse of AML but returned to 100% after successful therapy with 5-azacitidine and donor lymphocytes, and was sustained afterwards. HSCT, hematopoietic stem cell transplantation; AML, acute myeloid leukemia. b, In CCR5 genotyping with agarose gel electrophoresis of CCR5-PCR products, PBMC of the patient from month 35 after HSCT as well as in vitro generated HIV-1-specific CTL lines showed the homozygous CCR5Δ32 mutation. PBMC and B-cell lines from CCR5wt/wt, CCR5Δ32/wt, and CCR5Δ32/Δ32 individuals and a 50 bp DNA ladder served as controls. PBMC, peripheral blood mononuclear cells; wt, wildtype; RT, reverse transcriptase. c, CCR5 expression was lost from peripheral blood CD4+ T cells after HSCT in flow cytometric analyses. See also data from months 41–59 after HSCT for IciStem no. 19 as published in8. A reference range from a healthy cohort (n = 8) is given in grey as median with IQR. ART, antiretroviral therapy.
