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

Gandhi, Maher K., Moll, Guido, Smith, Corey, Dua, Ujjwal, Lambley, Eleanore, Ramuz, Olivier, Gill, Devinder, Marlton, Paula, Seymour, John F. and Khanna, Rajiv (2007) Galectin-1 mediated suppression of Epstein-Barr virus-specific T-cell immunity in classic Hodgkin lymphoma. Blood, 110 4: 1326-1329. doi:10.1182/blood-2007-01-066100


Author Gandhi, Maher K.
Moll, Guido
Smith, Corey
Dua, Ujjwal
Lambley, Eleanore
Ramuz, Olivier
Gill, Devinder
Marlton, Paula
Seymour, John F.
Khanna, Rajiv
Title Galectin-1 mediated suppression of Epstein-Barr virus-specific T-cell immunity in classic Hodgkin lymphoma
Journal name Blood   Check publisher's open access policy
ISSN 0006-4971
Publication date 2007
Sub-type Article (original research)
DOI 10.1182/blood-2007-01-066100
Volume 110
Issue 4
Start page 1326
End page 1329
Total pages 4
Editor S. J. Shattil
Place of publication USA
Publisher American Society of Hematology
Collection year 2008
Language eng
Subject 321008 Haematology
730103 Blood disorders
CX
Abstract 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.
Keyword Hematology
Expression
Disease
Responses
Death
Q-Index Code CX

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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Created: Tue, 22 Apr 2008, 15:36:42 EST by Denise Wilson on behalf of Medicine - Princess Alexandra Hospital