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P Fisch, G Weil-Hillman, M Uppenkamp, JA Hank, BP Chen, JA Sosman, A Bridges, OR Colamonici and PM Sondel
Department of Human Oncology, University of Wisconsin, Madison 53792.
Culturing of leukemic blood lymphocytes from a patient with acute T- cell
lymphoblastic leukemia (T-ALL) with interleukin-2 (IL-2) yielded T- cell
line AK-1 with a remarkable cytotoxic specificity. This line mediated
strong lysis of tumor target lines expressing major histocompatibility
complex (MHC) class I antigens, such as Raji, CEM, and Molt-4 cells, but no
killing of K562 and Daudi cells, which are deficient in MHC class I. In
contrast, lymphokine-activated killer (LAK) cells from normal donors
destroyed all these tumor targets, without MHC restriction. Line AK-1,
originating from residual normal T cells present in the leukemic blood,
lysed autologous leukemic blasts and peripheral blood lymphocytes (PBL)
from many but not all allogeneic individuals but failed to kill autologous
remission lymphocytes. Destruction of the autologous leukemic targets by
AK-1 could be inhibited by unlabeled competitor target cells that were
lysed by AK-1, but not by target cells that were not lysed. This suggests
that AK-1 specifically recognized an alien determinant on the autologous
ALL cells, crossreactive with allogeneic MHC class I antigens. This
reactivity with some degree of tumor specificity may be a leukemic
equivalent to responses reported for populations of tumor infiltrating
lymphocytes (TIL) seen in some solid tumors.
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