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Lymphokine-activated killer (LAK) cell activity in B and T chronic lymphoid
leukemia: defective LAK generation and reduced susceptibility of the
leukemic cells to allogeneic and autologous LAK effectors
R Foa, MT Fierro, D Raspadori, M Bonferroni, S Cardona, A Guarini, AG Tos, PF di Celle, A Cesano and L Matera
Dipartimento di Scienze Biomediche e Oncologia Umana, Sezione di Clinica
Medica, University of Torino, Italy.
The capacity to generate lymphokine-activated killer (LAK) cells and the
susceptibility of the neoplastic cells to both allogeneic and autologous
LAK effectors were studied in B and T chronic lymphoproliferative
disorders. While in B-cell chronic lymphocytic leukemia (B-CLL) the
depressed natural killer function could be restored after a 7-day
incubation with recombinant interleukin (IL-2), B-CLL mononuclear cells
showed a reduced LAK activity compared with normal LAK cells. Furthermore,
in all but 1 of the 20 B-CLL samples tested the leukemic cells were totally
resistant to autologous LAK effectors. In most cases the leukemic cells
were also resistant to normal allogeneic LAK cells. Competition experiments
demonstrated that the patients' LAK cells, as well as normal LAK effectors,
were capable of recognizing B-CLL cells, pointing, therefore, to a
postbinding cytolytic defect. In hairy cell leukemia (HCL) an overall
reduced LAK activity against allogeneic targets was documented, but, at
variance from B-CLL, hairy cells were often susceptible to the lytic effect
of normal LAK cells, and in half of the cases tested the neoplastic
population was also sensitive in an autologous system. Similarly to B- CLL,
in the great majority of T chronic lymphoproliferative disorders studied,
the pathologic cells were resistant to normal and autologous LAK effectors
and a defective LAK generation was found. These results demonstrate that in
most B and T chronic leukemias the LAK function is defective and, when
inducible, does not appear directed against the leukemic population. The
possibility of exploiting an immunotherapeutic approach with IL-2/LAK cells
in the management of chronic lymphoproliferative disorders does not gain
support by these findings.
Volume 76,
Issue 7,
pp. 1349-1354,
10/01/1990
Copyright © 1990 by The American Society of Hematology
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