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Carl B

Carl Borrebaeck

Professor

Carl B

Epstein-Barr virus-induced transformation of human B lymphocytes : the effect of l-leucyl-l-leucine methyl ester on inhibitory T cell populations

Author

  • M. Ohlin
  • K. Kristensson
  • R. Carlsson
  • C. A K Borrebaeck

Summary, in English

Epstein-Barr virus-mediated transformation of human B lymphocytes is inhibited by human T lymphocytes as well as by interferon-γ. Removal of the inhibitory cell populations is essential in order to achieve successful transformation in vitro. Cells with the capacity to inhibit outgrowth of lymphoblastoid cell lines can be removed by pretreatment of peripheral blood mononuclear cells with l-leucyl-l-leucine methyl ester. This treatment eliminates monocytes, NK-cells and a CD8+ T cell subpopulation. We now show that such treatment also has toxic effects on other human T cell populations. In addition, CD4+ and/or CD8+ lymphocytes are demonstrated to contain effector cell activities which inhibit outgrowth of EBV-transformed B cells. This inhibitory activity is abolished after treatment of peripheral blood mononuclear cells or purified CD4+ T cells with l-leucyl-l-leucine methyl ester. No evidence was found for a selective toxicity against any subset within the CD4+ or CD8+ T cell populations. However, the capacity of the treated cells, both peripheral blood mononuclear cells and purified CD4+ T lymphocytes, to produce mRNA encoding IFN-γ, a protein previously shown to downregulate outgrowth of EBV-transformed B cells, was selectively impaired. The results obtained suggest a role for CD4+ T cells to inhibit EBV-induced transformation of B cells.

Department/s

  • Department of Immunotechnology

Publishing year

1992

Language

English

Pages

221-228

Publication/Series

Immunology Letters

Volume

34

Issue

3

Document type

Journal article

Publisher

Elsevier

Topic

  • Immunology in the medical area

Keywords

  • B lymphocyte
  • Epstein-Barr virus
  • Interferon
  • l-Leucyl-l-leucine methyl ester
  • T lymphocyte
  • Transformation

Status

Published

ISBN/ISSN/Other

  • ISSN: 0165-2478