|
|
||||||||
Published online before print April 24, 2007
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
,1

* Departamento de Histologia e Embriologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil;
Laboratório de Oncologia Experimental, Faculdade de Medicina da Universidade de São Paulo, and Center for Cell-Based Therapy, CEPID-FAPESP, São Paulo, Brazil; and
Department of Dermatology, School of Medicine, University of California, Davis, Sacramento, California, USA
2 Correspondence: Universidade Federal do Rio de Janeiro, Av. Pau-Brasil, s/n, 21949-900 Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ, Brazil. E-mail: marcia{at}histo.ufrj.br
ABSTRACT
Galectin-3 (gal-3), a β-galactoside-binding animal lectin, plays a role in cell-cell and cell-extracellular matrix interactions. Extracellular gal-3 modulates cell migration and adhesion in several physiological and pathological processes. Gal-3 is highly expressed in activated macrophages. Schistosoma mansoni eggs display a large amount of gal-3 ligands on their surface and elicit a well-characterized, macrophage-dependent, granulomatous, inflammatory reaction. Here, we have investigated the acute and chronic phases of S. mansoni infection in wild-type and gal-3–/– mice. In the absence of gal-3, chronic-phase granulomas were smaller in diameter, displaying thinner collagen fibers with a loose orientation. Schistosoma-infected gal-3–/– mice had remarkable changes in the monocyte/macrophage, eosinophil, and B lymphocyte subpopulations as compared with the infected wild-type mice. We observed a reduction of macrophage number, an increase in eosinophil absolute number, and a decrease in B lymphocyte subpopulation (B220+/high cells) in the periphery during the evolution of the disease in gal-3–/– mice. B lymphopenia was followed by an increase of plasma cell number in bone marrow, spleen, and mesenteric lymph nodes of the infected gal-3–/– mice. The plasma IgG and IgE levels also increased in these mice. Gal-3 plays a role in the organization, collagen distribution, and mobilization of inflammatory cells to chronic-phase granulomas, niches for extramedullary myelopoiesis, besides interfering with monocyte-to-macrophage and B cell-to-plasma cell differentiation.
Key Words: Schistosoma mansoni plasma cells macrophages granuloma
This article has been cited by other articles:
![]() |
S. R. Stowell, C. M. Arthur, P. Mehta, K. A. Slanina, O. Blixt, H. Leffler, D. F. Smith, and R. D. Cummings Galectin-1, -2, and -3 Exhibit Differential Recognition of Sialylated Glycans and Blood Group Antigens J. Biol. Chem., April 11, 2008; 283(15): 10109 - 10123. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Breuilh, F. Vanhoutte, J. Fontaine, C. M. W. van Stijn, I. Tillie-Leblond, M. Capron, C. Faveeuw, T. Jouault, I. van Die, P. Gosset, et al. Galectin-3 Modulates Immune and Inflammatory Responses during Helminthic Infection: Impact of Galectin-3 Deficiency on the Functions of Dendritic Cells Infect. Immun., November 1, 2007; 75(11): 5148 - 5157. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |