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An HLA Lost Mutation May Lead to Leukemic Relapse of Recipient Type Six Years After Bone Marrow Transplantation

  • H. Grosse-Wilde
  • I. Doxiadis
  • U. Vögeler
  • H. K. Mahmoud
  • U. W. Schäfer
  • D. W. Beelen
  • H. L. Ploegh
Conference paper
Part of the Haematology and Blood Transfusion / Hämatologie und Bluttransfusion book series (HAEMATOLOGY, volume 30)

Abstract

Products of the major histocompatibility complex (MHC) serve to direct interactions amongst cells of the immune system. Cytolytic T cells recognize their targets by means of an antigen-specific receptor, but this recognition also requires a match of MHC antigens between effector and target cells (MHC restriction) [1]. Cytolytic T cells have been implicated in the elimination of malignantly transformed cells [2]. One mechanism by which tumor cells might escape immune destruction would be a reduction of the expression of MHC antigens, i.e., introduction of restriction elements. This situation occurs in cells transformed with an oncogenic strain of adenovirus which have switched off the expression of class I MHC antigens [3].

Keywords

Major Histocompatibility Complex Acute Myelogenous Leukemia Major Histocompatibility Complex Antigen Blood Group Typing Major Histocompatibility Complex Restriction 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Zinkernagel RM, Doherty PC (1975) H-2 compatibility requirement for T cell mediated lysis of target infected with lymphocytic choriomeningitis virus. Different cytotoxic T cell specificities are associated with structures coded in H2K or H-2D. J Exp Med 141: 1427–1436PubMedCrossRefGoogle Scholar
  2. 2.
    Bernards R, Schrier PI, Houweling A, Bos JL, van der Eb Ai (1983) Tumorigenicity of cells transformed by adenovirus type 12 by evasion of T-cell immunity. Nature 305: 776–779.PubMedCrossRefGoogle Scholar
  3. 3.
    Schrier PI, Bernards R, Vaessen RTMJ, Houveling A, van der Eb AJ (1983) Expression of class I major histocompatibility antigens switched off by highly oncogenic adenovirus 12 in transformed rat cells. Nature 305: 771–775PubMedCrossRefGoogle Scholar
  4. 4.
    Mahmoud HK, Schaefer UW, Schüning F, Schmidt CG, Grosse-Wilde H, Becher R, Luboldt W (1985) Late relapse of acute nonlymphoblastic leukaemia 6 years following allogeneic bone marrow transplantation. Br J Hematol 59: 731–732CrossRefGoogle Scholar
  5. 5.
    Parham P, Barnstable CJ, Bodmer WF (1979) Properties of an anti-HLA-A, -B, -C monoclonal antibody. Use of a monoclonal antibody (W6/32) in structural studies of HLA-A, -B, -C antigens. J Immunol 123: 242–247Google Scholar
  6. 6.
    Neefjes JJ, Breur-Vriesendorp BS, van Se-venter GA, Ivanyi P, Ploegh HL (1986) An improved biochemical method for the analysis of HLA-class I antigens. Definition of new HLAclass I subtypes. Hum Immunol 16: 169–181Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • H. Grosse-Wilde
    • 1
  • I. Doxiadis
    • 1
  • U. Vögeler
    • 1
  • H. K. Mahmoud
    • 2
  • U. W. Schäfer
    • 2
  • D. W. Beelen
    • 2
  • H. L. Ploegh
    • 3
  1. 1.Departments of Immunogenetics and Internal MedicineUniversity Hospital of EssenEssenFederal Republic of Germany
  2. 2.Tumor ResearchUniversity Hospital of EssenEssenFederal Republic of Germany
  3. 3.The Netherlands Cancer Institute AmsterdamThe Netherlands

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