BCR-ABL Is Not an Immunodominant Antigen in Chronic Myelogenous Leukemia

DOI PDF 被引用文献2件
  • Frank Grünebach
    Department of Hematology, Oncology, Immunology, and Rheumatology, University of Tübingen, Tübingen, Germany
  • Valbona Mirakaj
    Department of Hematology, Oncology, Immunology, and Rheumatology, University of Tübingen, Tübingen, Germany
  • Valdete Mirakaj
    Department of Hematology, Oncology, Immunology, and Rheumatology, University of Tübingen, Tübingen, Germany
  • Martin R. Müller
    Department of Hematology, Oncology, Immunology, and Rheumatology, University of Tübingen, Tübingen, Germany
  • Tim Brümmendorf
    Department of Hematology, Oncology, Immunology, and Rheumatology, University of Tübingen, Tübingen, Germany
  • Peter Brossart
    Department of Hematology, Oncology, Immunology, and Rheumatology, University of Tübingen, Tübingen, Germany

抄録

<jats:title>Abstract</jats:title> <jats:p>In the present study, we analyzed the involvement of the BCR-ABL protein in the induction of antigen-specific CTL in order to develop an immunotherapeutic approach in patients with chronic myelogenous leukemia (CML). To accomplish this, we generated dendritic cells (DC) in vitro and electroporated them with various sources of RNA harboring the chimeric bcr-abl transcript. These genetically engineered DCs were used as antigen-presenting cells for the induction of CTLs. By applying this approach, we found that the CTLs induced by DCs transfected with RNA extracted from bcr-abl–positive K-562 cells or CML blasts lysed DCs transfected with the corresponding RNA, but failed to recognize epitopes derived from the chimeric BCR-ABL fusion protein in 51Cr-release assays. In contrast, they were able to lyse autologous DCs electroporated with RNA isolated from patients with acute myeloid leukemia, indicating that antigens shared among these malignant cells are involved and recognized by these CTLs. In patients with CML in complete cytogenetic remission during IFN-α treatment, we detected some reactivity of CD8+ T cells against BCR-ABL in IFN-γ ELISPOT assays, which was weaker as compared with proteinase 3 (PR3)- or prame-directed responses, suggesting that the BCR-ABL protein is less immunogenic as compared with other CML-derived antigens. (Cancer Res 2006; 66(11): 5892-900)</jats:p>

収録刊行物

  • Cancer Research

    Cancer Research 66 (11), 5892-5900, 2006-06-01

    American Association for Cancer Research (AACR)

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