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Blood, 1 March 2004, Vol. 103, No. 5, pp. 1838-1845.
Prepublished online as a Blood First Edition Paper on October 30, 2003; DOI 10.1182/blood-2003-07-2440.
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NEOPLASIA
A neutralizing monoclonal antibody (mAb A24) directed against the transferrin receptor induces apoptosis of tumor T lymphocytes from ATL patients
Ivan C. Moura,
Yves Lepelletier,
Bertrand Arnulf,
Patrick England,
Cedric Baude,
Carole Beaumont,
Ali Bazarbachi,
Marc Benhamou,
Renato C. Monteiro, and
Olivier Hermine
From the Institut National de la Santé et de la Recherche Médicale (INSERM) E-0225, Faculté deMédecine Xavier Bichat, Paris, France; Centre National de Recherche Scientifique (CNRS) FRE-2444, Hôpital Necker, Paris, France; Plateforme de Biophysique des Macromolécules et de leurs Interactions, Institut Pasteur, Paris, France; INSERM U-409, Faculté de Médecine Xavier Bichat, Paris, France; Departments of Internal Medicine and Biochemistry, American University of Beirut, Beirut, Lebanon; and Department of Clinical Hematology, Hôpital Necker, Paris, France
Adult T-cell leukemia/lymphoma (ATL) is an aggressive lymphoid proliferative disease that exists under diverse clinical forms ranging from chronic to acute. Although leukemic cells from patients with ATL exhibit an intrinsic resistance to chemotherapy, monoclonal antibodies directed against CD25 (interleukin 2 receptor  [IL-2R] antibody) have been used as specific therapeutic agents. However, significant clinical results with these antibodies have been demonstrated only in chronic forms of ATL. In contrast to resting T cells, human T-cell lymphotropic virus type 1 (HTLV-1)–infected cells constitutively express high levels of surface transferrin receptor (TfR). Herein, we report the characterization of a new monoclonal antibody (mAb A24) directed against the human TfR and the evaluation of its capacity to block the proliferation of ATL cells ex vivo. We determined that A24 binds TfR with an equilibrium constant (K'd) of 2.7 nM and competes with transferrin for binding to TfR. A24 also inhibited [55Fe]-transferrin uptake in activated T cells and blocked T-cell proliferation. Moreover, A24 reduced and impaired TfR expression and recycling, respectively. Most important, we showed that A24 blocked the ex vivo proliferation of malignant T cells from both acute and chronic forms of ATL, through induction of programmed cell death. Therefore efficient therapeutic tools to treat acute forms of ATL might be derived from A24.
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