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CD4 T-Helper Responses to the Anaplastic Lymphoma Kinase (ALK) Protein in Patients with ALK-Positive Anaplastic Large-Cell Lymphoma

¹ Nuffield Department of Clinical Laboratory Sciences, Leukemia Research Fund Immunodiagnostics Unit, John Radcliffe Hospital, and ² Transplant Immunology, Oxford Transplant Center, Churchill Hospital, Oxford, United Kingdom

Requests for reprints: Kamel Ait-Tahar, Nuffield Department of Clinical Laboratory Sciences, Leukemia Research Fund Lymphoma Antigens Group, Room 5501, Level 5, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom. Phone: 44-1865-220536-222913; Fax: 44-1865-222912; E-mail: kamel.ait-tahar{at}ndcls.ox.ac.uk.

We have previously shown both humoral and CTL responses to anaplastic lymphoma kinase (ALK) in patients with ALK-positive anaplastic large-cell lymphoma (ALCL). However, because CD4⁺ T-helper (Th) cells also play a vital role in developing and maintaining tumor immunity, we investigated the presence of a CD4⁺ Th response in ALK-positive ALCL. Using an IFN- ELISPOT assay, we identified two ALK-derived DRB1-restricted 24-mer promiscuous peptides, ALK1_278–301 and ALK2_233–256, as being immunogenic in six ALK-positive ALCL patients but not in two ALK-negative ALCL patients or five normal subjects. A significant interleukin-4 response to the ALK peptides was detected in only one ALK-positive patient. CD4⁺ Th cell lines lysed ALK-positive ALCL cell lines in a MHC class II–restricted manner. This first report of a CD4⁺ Th response to ALK provides valuable information for developing future immunotherapeutic options for ALK-positive ALCL patients who fail to respond well to conventional therapies. [Cancer Res 2007;67(5):1898–901]