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 Blood, 15 August 2007, Vol. 110, No. 4, pp. 1326-1329.
Prepublished online as a Blood First Edition Paper on April 16, 2007; DOI 10.1182/blood-2007-01-066100.

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NEOPLASIA

Brief Report

Galectin-1 mediated suppression of Epstein-Barr virus–specific T-cell immunity in classic Hodgkin lymphoma

Maher K. Gandhi1,3, Guido Moll1, Corey Smith1, Ujjwal Dua1, Eleanore Lambley1, Olivier Ramuz2, Devinder Gill3, Paula Marlton3, John F. Seymour4, and Rajiv Khanna1

1 Australian Centre for Vaccine Development, Tumor Immunology Laboratory, Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane; 2 Molecular and Cellular Pathology, School of Medicine, University of Queensland, Brisbane; 3 Department of Haematology, Princess Alexandra Hospital, Brisbane; and 4 Haematology Service, Peter MacCallum Cancer Centre, and University of Melbourne, Melbourne, Australia

In Hodgkin lymphoma (HL), the malignant Hodgkin Reed-Sternberg cells interact with the host microenvironment to create an immunosuppressive network that protects the lymphoma from immune attack. These mechanisms are not fully understood. We examined the role of the immunomodulatory protein galectin-1 (Gal-1) on Epstein-Barr virus-specific CD8+ T cell responses in HL. Initial studies indicated Gal-1 expression in all in vitro established Hodgkin Reed-Sternberg cell lines. In situ analysis revealed Gal-1 expression in 26 of 42 classic HL, whereas Gal-1 was uniformly negative in nodular lymphocyte predominant HL. Gal-1hi expression was associated with male gender, older patients, reduced CD8+ T cell infiltration at the tumor site, and most importantly, an impaired latent membrane protein 1 and 2-specific CD8+ T-cell responses. In vitro exposure to recombinant Gal-1 inhibited proliferation and interferon-{gamma} expression by Epstein-Barr virus-specific T cells. These observations provide an important link between the Gal-1-mediated immunomodulatory networks and loss of antigen-specific T-cell function in classic HL.


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