© 2003 BMJ Publishing Group & Association of Clinical Pathologists
EDITORIAL
Immune escape
Immune escape mechanisms in ALCL
Department of Pathology, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands
Correspondence to:
Correspondence to:
Dr J J Oudejans, VU University Medical Centre, Department of Pathology, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands;
jj.oudejans@vumc.nl
Why do host T cells not recognise and eradicate anaplastic large cell lymphomas?
Keywords: anaplastic large cell lymphoma; cytotoxic T cell; apoptosis; major histocompatibility complex; serine protease inhibitor; protease inhibitor 9
| The first 150 words of the full text of this article appear below. |
Systemic anaplastic large cell lymphoma (ALCL) is a CD30 positive T cell lymphoma with a broad spectrum of morphological, immune phenotypical, and clinical characteristics.1 Two clinicopathological entities can be distinguished: anaplastic lymphoma kinase (ALK) positive systemic nodal ALCL and ALK negative systemic nodal ALCL. ALK expression, usually the result of a t(2;5) translocation, is related to a younger age, lower international prognostic index risk, and an excellent prognosis.2–4 Similar to most other lymphomas, ALCLs harbour many non-neoplastic, in principle immune competent, lymphocytes. In immune competent patients, putative expression of tumour antigens in ALCL (or any other lymphoma) should, in principle, elicit an antitumour immune response. Indeed, it was shown recently that ALK can elicit a humoral antitumour immune response in ALK positive patients with ALCL and that functional anti-ALK CTL precursors are present within the peripheral T cell repertoire of healthy donors, clearly indicating that ALK is a
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