Figure 5.
Incidence of acute GVHD correlates with increased IFN-γ production by donor-derived NK cells. Cumulative incidence estimates of acute GVHD in recipients of UBM or TCD transplants are shown. The percentage of day +100, donor-derived recipient CD3-/CD56+ NK cells producing IFN-γ was analyzed as described, and the results were analyzed with a Cox multivariate proportionate hazards model that included KIR expression, percentage of CD56+bright cells, graft type, IFN-γ production, and the incidence of acute GVHD. The recipients were further stratified by IFN-γ production by equal to or more than 50% or less than 50% of NK cells, which was the mean percentage of NK cells producing IFN-γ for all samples (left panel). The type of graft (UBM or TCD) did not independently correlate with acute GVHD but did accentuate the effect of IFN-γ expression (right panel).

Incidence of acute GVHD correlates with increased IFN-γ production by donor-derived NK cells. Cumulative incidence estimates of acute GVHD in recipients of UBM or TCD transplants are shown. The percentage of day +100, donor-derived recipient CD3-/CD56+ NK cells producing IFN-γ was analyzed as described, and the results were analyzed with a Cox multivariate proportionate hazards model that included KIR expression, percentage of CD56+bright cells, graft type, IFN-γ production, and the incidence of acute GVHD. The recipients were further stratified by IFN-γ production by equal to or more than 50% or less than 50% of NK cells, which was the mean percentage of NK cells producing IFN-γ for all samples (left panel). The type of graft (UBM or TCD) did not independently correlate with acute GVHD but did accentuate the effect of IFN-γ expression (right panel).

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