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Endogenous lymphokine activated killer cell activity and cytogenetic response in chronic myelogenous leukaemia

A Meseri1, V Delwail, A Brizard

  • 1URA C.N.R.S. 1338, Centre de Recherches sur les Maladies du Sang, Université de Poitiers, France.

British Journal of Haematology
|February 1, 1993
PubMed

Insights

Alpha-interferon (alpha-IFN) therapy may enhance chronic myelogenous leukaemia (CML) remission by boosting natural killer (NK) and lymphokine-activated killer (LAK) cell activity. This suggests an indirect immune surveillance mechanism for alpha-IFN in CML treatment.

Area of Science:

  • Immunology
  • Hematology
  • Oncology

Background:

  • Alpha-interferon (alpha-IFN) can induce lymphokine-activated killer (LAK) cytotoxicity independently of interleukin-2 (IL2).
  • The mechanism by which alpha-IFN reduces Philadelphia chromosome-positive (Ph1+) clones in chronic myelogenous leukaemia (CML) is not fully understood.

Purpose of the Study:

  • To investigate if alpha-interferon's efficacy in CML treatment is mediated by the generation of natural killer (NK) or LAK activity.
  • To correlate NK/LAK activity with cytogenetic remission in CML patients undergoing alpha-IFN therapy.

Main Methods:

  • NK and LAK cytotoxicity were assessed using NK-sensitive (K562) and NK-resistant (Raji) cell lines in a colony-growth inhibition assay.
  • Effector cells were patient blood mononuclear cells (MC) without in vitro activation.
  • 16 CML patients treated with alpha-IFN were evaluated.

Main Results:

  • Thirteen of 16 patients achieved complete or partial cytogenetic remission, exhibiting significantly high NK and/or LAK activity compared to normal controls.
  • Two patients who did not achieve remission showed no detectable NK or LAK cells, while one had NK activity within normal limits.
  • No NK or LAK cells were detected in two non-remitting patients.

Conclusions:

  • The findings support the hypothesis that alpha-interferon exerts an indirect effect on CML cells.
  • This indirect effect may be mediated by immune surveillance mechanisms involving NK and LAK cells.
  • Alpha-IFN therapy could enhance CML remission through the induction of anti-leukaemic immune responses.

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