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Activation signals leading to proliferation of normal and leukemic CD3+ large granular lymphocytes

J A Aprile1, M Russo, M S Pepe

  • 1Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.

Blood
|September 11, 1991
PubMed

Insights

Normal and leukemic CD3+ large granular lymphocytes (LGL) proliferate in vitro. Activation signals including anti-CD3 monoclonal antibody and interleukin-2 directly stimulate leukemic LGL proliferation.

Area of Science:

  • Immunology
  • Hematology
  • Cell Biology

Background:

  • CD3+ large granular lymphocytes (LGL) are involved in immune responses.
  • Understanding the proliferation signals of normal and leukemic LGL is crucial for therapeutic strategies.

Purpose of the Study:

  • To investigate the in vitro activation signals that induce proliferation of normal and leukemic CD3+ LGL.
  • To determine the role of T-cell receptor and lymphokine signaling in LGL proliferation.

Main Methods:

  • Peripheral blood mononuclear cells (PBMC) from LGL leukemia patients were cultured with anti-CD3 monoclonal antibody (MoAb) and/or recombinant interleukin-2 (IL-2) or interleukin-4 (IL-4).
  • Proliferation was measured using a 3H-thymidine incorporation assay.
  • Purified leukemic LGL were assessed for cell cycle entry (S + G2/M phase) using Hoechst staining after activation.

Main Results:

  • Both anti-CD3 MoAb and IL-2 alone significantly stimulated PBMC proliferation (P < .01).
  • Recombinant IL-4 alone had no significant effect (P = .11).
  • Combined anti-CD3 MoAb with IL-2 or IL-4 resulted in greater proliferation than either stimulus alone (P < .01).
  • Purified leukemic LGL showed direct stimulation by anti-CD3 MoAb and IL-2, with 16%-72% entering the cell cycle.
  • Normal CD3+ LGL also entered the cell cycle upon stimulation with anti-CD3 and IL-2.

Conclusions:

  • Leukemic LGL proliferate in vitro upon activation through the T-cell receptor and/or lymphokine signaling pathways.
  • Anti-CD3 MoAb and IL-2 are potent stimulators of both normal and leukemic CD3+ LGL proliferation.
  • These findings highlight the potential for targeting these pathways in LGL leukemia treatment.

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