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Prepublished online as a Blood First Edition Paper on July 5, 2002; DOI 10.1182/blood-2002-04-1041.
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Blood, 1 November 2002, Vol. 100, No. 9, pp. 3155-3163
GENE THERAPY
Single-chain antigen recognition receptors that costimulate
potent rejection of established experimental tumors
Nicole M. Haynes,
Joseph A. Trapani,
Michèle W. L. Teng,
Jacob T. Jackson,
Loretta Cerruti,
Stephen M. Jane,
Michael H. Kershaw,
Mark J. Smyth, and
Phillip K. Darcy
From the Cancer Immunology Program, Sir Donald and Lady
Trescowthick Laboratories, Peter MacCallum Cancer Institute, and the
Rotary Bone Marrow Research Laboratory, Royal Melbourne Hospital
Research Foundation, Victoria, Australia.
Tumor cells are usually weakly immunogenic as they largely express
self-antigens and can down-regulate major histocompatability complex/peptide molecules and critical costimulatory ligands. The
challenge for immunotherapies has been to provide vigorous immune
effector cells that circumvent these tumor escape mechanisms and
eradicate established tumors. One promising approach is to engineer T
cells with single-chain antibody receptors, and since T cells require 2 distinct signals for optimal activation, we have compared the
therapeutic efficacy of erbB2-reactive chimeric receptors that contain
either T-cell receptor zeta (TCR- ) or CD28/TCR- signaling
domains. We have demonstrated that primary mouse CD8+ T
lymphocytes expressing the single-chain Fv (scFv)-CD28- receptor have a greater capacity to secrete Tc1 cytokines, induce T-cell proliferation, and inhibit established tumor growth and metastases in
vivo. The suppression of established tumor burden by cytotoxic T cells
expressing the CD28/TCR- chimera was critically dependent upon their
interferon gamma (IFN- ) secretion. Our study has illustrated the
practical advantage of engineering a T-cell signaling complex that
codelivers CD28 activation, dependent only upon the tumor's expression
of the appropriate tumor associated antigen.
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