Downregulation of HLA class II is associated with relapse after allogeneic stem cell transplantation and alters recognition by antigen-specific T cells.
Yoshitaka AdachiToshiyasu SakaiSeitaro TerakuraTakashi ShiinaShingo SuzukiHiroshi HamanaHiroyuki KishiTakehiko SasazukiHisashi AraseRyo HanajiriTatsunori GotoTetsuya NishidaMakoto MurataHitoshi KiyoiPublished in: International journal of hematology (2022)
Genomic deletion of donor-patient-mismatched HLA alleles in leukemic cells is a major cause of relapse after allogeneic hematopoietic stem cell transplantation (HSCT). Mismatched HLA is frequently lost as an individual allele or a whole region in HLA-class I, however, it is downregulated in HLA-class II. We hypothesized that there might be a difference in T cell recognition capacity against epitopes associated with HLA-class I and HLA-class II and consequently such allogeneic immune pressure induced HLA alterations in leukemic cells. To investigate this, we conducted in vitro experiments with T cell receptor-transduced T (TCR-T) cells. The cytotoxic activity of NY-ESO-1-specific TCR-T cells exhibited similarly against K562 cells with low HLA-A*02:01 expression. However, we demonstrated that the cytokine production against low HLA-DPB1*05:01 expression line decreased gradually from the HLA expression level approximately 2-log lower than normal expressors. Using sort-purified leukemia cells before and after HSCT, we applied the next-generation sequencing, and revealed that there were several marked downregulations of HLA-class II alleles which demonstrated consistently low expression from pre-transplantation. The marked downregulation of HLA-class II may lead to decreased antigen recognition ability of antigen-specific T cells and may be one of immune evasion mechanism associated with HLA-class II downregulation.
Keyphrases
- endoplasmic reticulum stress
- induced apoptosis
- stem cell transplantation
- poor prognosis
- acute myeloid leukemia
- allogeneic hematopoietic stem cell transplantation
- bone marrow
- high dose
- signaling pathway
- binding protein
- cell proliferation
- stem cells
- case report
- immune response
- acute lymphoblastic leukemia
- regulatory t cells
- single cell
- stress induced
- endothelial cells
- diabetic rats