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Induction of CD11a/leukocyte function antigen-1 and CD54/intercellular
adhesion molecule-1 on hairy cell leukemia cells is accompanied by enhanced
susceptibility to T-cell but not lymphokine-activated killer- cell
cytotoxicity [see comments]
JH Jansen, D van der Harst, GJ Wientjens, YM Kooy-Winkelaar, A Brand, R Willemze and HC Kluin-Nelemans
Department of Hematology, University Medical Center, Leiden, The
Netherlands.
Some B-cell neoplasms, including hairy cell leukemia (HCL), lack expression
of the adhesion molecule leukocyte function antigen-1 (LFA- 1/CD11a).
Additionally, HCL cells express relatively low amounts of intercellular
adhesion molecule-1 (ICAM-1/CD54) and may therefore be an inappropriate
target for recognition by T cells or lymphokine-activated killer (LAK)
cells. We tested whether these molecules were inducible on HCL cells and if
induction would lead to enhanced susceptibility to lysis by LAK cells or
cytolytic T cells. CD11a expression was induced by incubation with
interferon-alpha (IFN-alpha) or interleukin-4. CD54 was induced by
culturing the cells irrespectively of the addition of cytokines. Expression
of CD11a and CD54 did not enhance susceptibility to either autologous or
allogeneous LAK cells. However, induction of these adhesion molecules was
accompanied by enhanced susceptibility to lysis by cytotoxic T lymphocyte
clones. This lysis could be reversed by the addition of anti-CD11a and
anti-CD54 antibodies. Finally, we monitored the expression of CD11a and
CD54 on HCL cells from patients during IFN-alpha therapy. In one of four
patients monitored, we observed rapid in vivo induction of CD11a and CD54
on the leukemic cells during IFN-alpha therapy. These studies provide a
model for studying immunosurveillance in HCL.
Volume 80,
Issue 2,
pp. 478-483,
07/15/1992
Copyright © 1992 by The American Society of Hematology
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