Figure 4.
Figure 4. The increased GVHD risk after unrelated HCT is predominantly an effect of HLA-mismatching. Panels compare the cumulative incidence frequencies of GVHD-related outcomes for sibling recipients, HLA 16/16–matched unrelated recipients, and HLA-DP GVH-mismatched unrelated recipients. Results are shown for (A) grades II-IV GVHD, (B) grades IIb-IV GVHD (see “Methods”), (C) grades III-IV GVHD, (D) stages 2-4 gut GVHD, (E) extensive chronic GVHD, and (F) the competing risks of nonrelapse mortality or recurrent or progressive malignancy. The higher incidence of competing risks in the HLA 16/16–matched unrelated recipients is entirely attributable to a higher incidence of recurrent or progressive malignancy (see Figure 5A). DP, HLA-DP; URD, unrelated donor.

The increased GVHD risk after unrelated HCT is predominantly an effect of HLA-mismatching. Panels compare the cumulative incidence frequencies of GVHD-related outcomes for sibling recipients, HLA 16/16–matched unrelated recipients, and HLA-DP GVH-mismatched unrelated recipients. Results are shown for (A) grades II-IV GVHD, (B) grades IIb-IV GVHD (see “Methods”), (C) grades III-IV GVHD, (D) stages 2-4 gut GVHD, (E) extensive chronic GVHD, and (F) the competing risks of nonrelapse mortality or recurrent or progressive malignancy. The higher incidence of competing risks in the HLA 16/16–matched unrelated recipients is entirely attributable to a higher incidence of recurrent or progressive malignancy (see Figure 5A). DP, HLA-DP; URD, unrelated donor.

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