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Infection and Immunity, November 2007, p. 5148-5157, Vol. 75, No. 11
0019-9567/07/$08.00+0     doi:10.1128/IAI.02006-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Galectin-3 Modulates Immune and Inflammatory Responses during Helminthic Infection: Impact of Galectin-3 Deficiency on the Functions of Dendritic Cells{triangledown}

Laetitia Breuilh,1,2,3,5,{dagger} François Vanhoutte,1,2,3,{dagger} Josette Fontaine,1,2,3 Caroline M. W. van Stijn,4 Isabelle Tillie-Leblond,1,2,5 Monique Capron,1,2,3 Christelle Faveeuw,1,2,3 Thierry Jouault,3,6 Irma van Die,4 Philippe Gosset,1,2,5 and François Trottein1,2,3*

Institut National de la Recherche Médicale, U547,1 Institut Pasteur de Lille, Institut Fédératif de Recherche 142,2 Université de Lille 2, Lille, F-59019 France,3 VU University Medical Center, 1081 BT Amsterdam, The Netherlands,4 Inserm U774, Lille, F-59019 France,5 Inserm U799, Lille, F-59037 France6

Received 22 December 2006/ Returned for modification 10 February 2007/ Accepted 21 August 2007

Galectin-3 (Gal-3) is a multifunctional ß-galactoside-binding lectin that senses self-derived and microbial glycoconjugates. Although Gal-3 is important in immune reactions and host defense in some experimental models, the function of Gal-3 during helminthic diseases (e.g., schistosomiasis) is still elusive. We show that, compared to wild-type Schistosoma mansoni-infected mice, infected Gal-3–/– mice have a reduced number of T and B lymphocytes in the spleen, develop reduced liver granulomas at 7 weeks (acute phase) and 14 weeks (chronic phase) postinfection, and mount a biased cellular and humoral Th1 response. In an attempt to understand this latter phenomenon, we studied the role of endogenous Gal-3 in dendritic cells (DCs), the most potent antigen-presenting cells, both in vitro and in vivo. Although Gal-3 deficiency in DCs does not impact their differentiation and maturation processes, it greatly influences the strength (but not the nature) of the adaptive immune response that they trigger, suggesting that Gal-3 deficiency in some other cell types may be important during murine schistosomiasis. As a whole, this study implies that Gal-3 is a modulator of the immune/inflammatory responses during helminthic infection and reveals for the first time that Gal-3 expression in DCs is pivotal to control the magnitude of T-lymphocyte priming.

* Corresponding author. Mailing address: Unité Inserm U547, Institut Pasteur de Lille, 1 rue du Professeur Calmette, 59019 Lille Cedex, France. Phone: (333) 2087-7885. Fax: (333) 2087-7888. E-mail: fran%E7ois.trottein{at}pasteur-lille.fr

{triangledown} Published ahead of print on 4 September 2007.

Editor: J. F. Urban, Jr.

{dagger} L.B. and F.V. contributed equally to this work.

Infection and Immunity, November 2007, p. 5148-5157, Vol. 75, No. 11
0019-9567/07/$08.00+0     doi:10.1128/IAI.02006-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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