Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 123, Issue 12, Pages 2824-2831Publisher
WILEY-BLACKWELL
DOI: 10.1002/ijc.23845
Keywords
EBNA1; CD4(+) T cells; Hodgkin's lymphoma
Categories
Funding
- National Cancer Institute [R01CA108609, R01CA101741]
- National Institute of Allergy and Infectious diseases [RFP-NIH-NIAID-DAIDS-BAA-06-19]
- Arnold and Mabel Beckman Foundation
- Alexandrine and Alexander Sinsheimer Foundation
- Burroughs Wellcome Fund
- Starr Foundation
- Foundation for the National Institutes of Health (Grand Challenges in Global Health)
- Children's Cancer Research Fund
- National Center for Research Resources [UL1-RR024143]
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Epstein Barr virus (EBV) causes lymphomas in immune competent and, at increased frequencies, in immune compromised patients. In the presence of an intact immune system, EBV-associated lymphomas express in most cases only 3 or fewer EBV antigens at the protein level, always including the nuclear antigen 1 of EBV (EBNA1). EBNA1 is a prominent target for EBV-specific CD4(+) T cell and humoral immune responses in healthy ERV carriers. Here we demonstrate that patients with EBV-associated lymphomas, primarily Hodgkin's lymphoma, lack detectable EBNA1-specific CD4(+) T-cell response's and have slightly altered EBNA1-specific antibody titers at diagnosis. In contrast, the majority of EBV-negative lymphoma patients had detectable IFN gamma expression and proliferation by CD4(+) T cells in response to EBNA1, and carry EBNA1-specific immunoglobulins at levels similar to healthy virus carriers. Other EBV antigens, which were not present in the tumors, were recognized in less EBV positive, than negative lymphoma patients, but detectable responses reached similar CD8(+) T cell frequencies in both cohorts. Patients with EBV-positive and -negative lymphomas did not differ in T-cell responses in influenza-specific CD4(+) T cell proliferation and in antibody titers against tetanus toxoid. These data suggest a selective loss of EBNA1-specific immune control in EBV-associated lymphoma patients, which should be targeted for immunotherapy 4 these malignancies. (C) 2008 Wiley-Liss, Inc.
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