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Cytotoxicity of interleukin 2-activated lymphocytes for leukemia and
lymphoma cells
K Oshimi, Y Oshimi, M Akutsu, Y Takei, H Saito, M Okada and H Mizoguchi
Studies were undertaken to determine whether leukemia and lymphoma cells
would be lysed by autologous and allogeneic lymphokine-activated killer
(LAK) cells. Peripheral blood mononuclear cells (PBMC) from patients and
normal donors were cultured for five days, 2 weeks, and 4 weeks with medium
containing 2,500 units of recombinant interleukin 2 (IL-2) per mL, and
their cytotoxicity was assayed by a five-hour 51Cr- release test. Of
primary tumors isolated from patients with acute nonlymphoblastic leukemia,
acute lymphoblastic leukemia, and non- Hodgkin's lymphoma, tumors of 37 out
of 40 patients tested were shown to be susceptible to normal donors' LAK,
and tumors of 18 of 20 patients tested were shown to be susceptible to
autologous LAK. LAK cultured for longer periods showed a tendency to have
lower cytotoxicity. LAK had also low, but significant, levels of
cytotoxicity for nonmalignant target cells. Because PBMC expanded in
IL-2-containing medium consisted mainly of OKT3-positive pan T cells,
OKT8-positive suppressor/cytotoxic cells, and Leu-11-positive natural
killer (NK) cells, and treatment with OKT3 and Leu-11 monoclonal antibodies
(mAb) reduced LAK activity for autologous and allogeneic tumor cells, both
T and NK cells appeared to be effector cells for LAK activity. Mechanisms
of target-cell recognition in the LAK system seem to be different from
those in alloreactive cytotoxic T lymphocytes (CTL) based on the results
that, while cytotoxicity of alloreactive CTL was inhibited by the treatment
of effector cells with mAb, OKT3, and OKT8, and by the treatment of target
cells with a mAb that reacts with HLA class I antigen, LAK activity was not
inhibited by the above treatment. When chromosomes of IL-2-expanded PBMC in
nine patients and two normal individuals were analyzed, PBMC from one
patient showed chromosomes of clonal abnormalities, and PBMC from five
donors showed those of nonclonal abnormalities.
Volume 68,
Issue 4,
pp. 938-948,
10/01/1986
Copyright © 1986 by The American Society of Hematology
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