Immune Escape of AML Cells after Transplantation

Abstract

1 investigating immune escape of relapsed acute myeloid leukemia (AML) cells after allogeneic transplantation, half the patients (17 of 34 patients evaluated with post-transplantation relapse) had decreased expression of major histocompatibility complex (MHC) class II proteins that was identified by means of flow cytometry. We think that the authors may have missed a possible role for viral-mediated MHC down-regulation, such as by means of Epstein-Barr virus (EBV) virally encoded micro-RNAs. 2 In addition, the EBV-encoded late lytic protein BDLF3 involves ubiquitination and prote-asome-dependent down-regulation of surface MHC class II molecules. 3 Other viruses, such as human herpesvirus 8 (HHV-8), also encode proteins , lytic transactivator RTA, and MARCH8, which mediate class II HLA-DRα down-regulation. 4 The data provided in Table S7 in the Supplementary Appendix (available with the full text of the article at NEJM.org) support a potential role for viral-mediated down-regulation. The use of selective HLA class II antibodies, rather than a panspecific antibody, could help to identify such effects. Appropriate antiviral interventions may be a quicker strategy to resensitize AML cells to the graft-versus-leukemia effect.