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Anti-CD3 monoclonal antibody-mediated cytotoxicity occurs through an
interleukin-2-independent pathway in CD3+ large granular lymphocytes
TP Loughran , JA Aprile and FW Ruscetti
Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
The mechanism of induction of cytotoxicity produced by anti-CD3 monoclonal
antibody (MoAb) was studied in four patients with CD3+ large granular
lymphocyte (LGL) leukemia. Anti-CD3 MoAb treatment resulted in increased
target cell binding and increased granule formation. After activation,
leukemic LGL remained Tac-, with the exception of a patient with CD4+ LGL
leukemia. Radiolabeled interleukin-2 (IL-2) binding studies demonstrated
that treatment with anti-CD3 MoAb resulted in upregulation of the number of
p75 intermediate affinity IL-2 receptor sites per cell. Northern blot
hybridization analysis showed expression of gamma-interferon gene
transcripts 24 to 48 hours after activation. There was no evidence for
expression of IL-2 messenger RNA or secretion of IL-2 after activation.
Anti-CD3 MoAb and IL-2 provide different signals for activation of CD3+
LGL. Induction of cytotoxicity produced by anti-CD3 MoAb in leukemic CD3+
LGL is not associated with IL-2 production.
Volume 75,
Issue 4,
pp. 935-940,
02/15/1990
Copyright © 1990 by The American Society of Hematology
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