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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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Submitted January 8, 2007
Accepted April 11, 2007
Galectin-1 mediated suppression of EBV-specific T-cell immunity in classical Hodgkin's Lymphoma
Maher K Gandhi, Guido Moll, Corey Smith, Ujjwal Dua, Eleanore Lambley, Olivier Ramuz, Devinder Gill, Paula Marlton, John F Seymour, and Rajiv Khanna*
Division of Infectious Diseases & Immunology, Australian Centre for Vaccine Development, Tumor Immunology Laboratory, QIMR, Brisbane, Australia
Molecular & Cellular Pathology, School of Medicine, The University of Queensland, Brisbane, Australia
Department of Haematology, Princess Alexandra Hospital, Brisbane, Australia
Haematology Service, Peter MacCallum Cancer Centre, University of Melbourne, Melbourne, Australia
* Corresponding author; email: rajivk{at}qimr.edu.au.
In Hodgkin's Lymphoma (HL), the malignant Hodgkin Reed-Sternberg (HRS) 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 EBV-specific CD8+ T-cell responses in HL. Initial studies indicated Gal-1 expression in all in-vitro established HRS cell-lines. In-situ analysis revealed Gal-1 expression in 26 of 42 classical HL (cHL), while 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 tumour site and most importantly an impaired latent membrane protein 1 & 2-specific CD8+ T-cell responses. In-vitro exposure to recombinant Gal-1 inhibited proliferation and IFN- expression by EBV-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 cHL.
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