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Acquired erythropoietin responsiveness of interleukin-2-dependent T
lymphocytes retrovirally transduced with genes encoding chimeric
erythropoietin/interleukin-2 receptors
S Minamoto, J Treisman, WD Hankins, K Sugamura and SA Rosenberg
Surgery Branch, National Cancer Institute, National Institutes of Health,
Bethesda, MD 20892, USA.
Adoptive immunotherapy with tumor-infiltrating lymphocytes (TILs) causes
regression of some human tumors. However, the sustained proliferation and
antitumor activity of TILs requires the coadministration of potentially
toxic amounts of interleukin-2 (IL-2). In an effort to overcome the
requirement by T cells for IL-2, we have introduced alternative growth
factor receptors that use the relatively nontoxic cytokine erythropoietin
(Epo) as a ligand. In our model system, the coexpression of chimeric
receptors consisting of the extracellular portion of the Epo receptor
(EpoR) and the intracellular portions of the IL-2 receptor subunits, beta
and gamma, conferred Epo responsiveness on a T-cell line. By contrast,
cells expressing the wild- type EpoR did not proliferate in response to
Epo. This suggested that Epo binding caused the activation of an IL-2
signal pathway mediated by the chimeric receptors. This approach can be
used to minimize toxicity and potentially improve cancer immunotherapy with
TILs.
Volume 86,
Issue 6,
pp. 2281-2287,
09/15/1995
Copyright © 1995 by The American Society of Hematology
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