Nematode galectin binds IgE and modulates mast cell activity

Mast cell degranulation is the major mechanism influencing establishment and survival of the abomasal nematode Teladorsagia circumcincta and probably many other gastrointestinal nematodes. Host galectins-3 and -9 have been shown to bind IgE and positively and negatively influence mast cell degranula...

Full description

Saved in:
Bibliographic Details
Published in:Veterinary parasitology Vol. 311; p. 109807
Main Authors: Donskow-Łysoniewska, Katarzyna, Maruszewska-Cheruiyot, Marta, Krawczak-Wójcik, Katarzyna, Gonzalez, Jorge F., Hernández, Julia N., Stear, Michael J.
Format: Journal Article
Language:English
Published: Elsevier B.V 01-11-2022
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Mast cell degranulation is the major mechanism influencing establishment and survival of the abomasal nematode Teladorsagia circumcincta and probably many other gastrointestinal nematodes. Host galectins-3 and -9 have been shown to bind IgE and positively and negatively influence mast cell degranulation. As incoming nematodes produce large amounts of galectin, we hypothesised that nematode galectin competes with host galectin and inhibits mast cell degranulation. ELISA was used to show that nematode galectin reduced total IgE activity. Galectin also reduced the binding of sheep IgE to the surface of a mast cell line and decreased the release of LCT-4 and Beta hexosaminidase but not MMP-9. These results indicate that nematode galectin influences mast cell degranulation and identify a potential immunomodulatory mechanism used by nematodes to enhance their establishment and survival. [Display omitted] •Sheep from a resistant breed had higher IgE anti-galectin activity than susceptible sheep.•Nematode galectin binds IgE and reduces apparent IgE concentrations.•Nematode galectin inhibits mast cell degranulation.•Nematodes produce galectin to enhance their establishment and survival.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0304-4017
1873-2550
DOI:10.1016/j.vetpar.2022.109807