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Lack of galectin‐3 involvement in murine intestinal nematode and schistosome infection
Author(s) -
BICKLE Q.,
HELMBY H.
Publication year - 2007
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2006.00923.x
Subject(s) - biology , immunology , heligmosomoides polygyrus , schistosoma mansoni , immune system , helminths , granuloma , antigen , galectin , epitope , schistosomiasis , helminthiasis , immunoglobulin e , antibody , hygiene hypothesis
SUMMARY Many parasitic helminths produce large quantities of glycosylated proteins, some if which are believed to be involved in the skewing towards the dominant Th2 response observed during helminth infection. Galectin‐3 is a member of a family of lectin‐binding proteins produced by many different types of immune cells, including macrophages. Galectin‐3 recognizes the GalNAcβ1‐4GlcNAc (LDN) epitope present on many helminth antigens, including those of the schistosome eggs. Here we show that galectin‐3 is not involved in the development of the Th2 response nor in schistosome granuloma formation. Galectin‐3‐deficient mice were able to expel the gastrointestinal nematode Trichuris muris at the same speed as wild‐type mice. Expulsion of T. muris is known to be dependent on a Th2 immune response and galectin‐3‐deficient mice showed no defect in their ability to produce Th2 cytokines or in their antibody responses, compared to wild‐type mice. Furthermore, galectin‐3‐deficient mice were also able to mount a Th2 response to Schistosoma mansoni infection and they exhibited normal hepatic granuloma formation. The data presented here demonstrate that galectin‐3 is not a critical component in the development of Th2 responses during helminth infection in vivo , nor is it essential for schistosome egg granuloma formation.