Altered expression of genes related to innate antifungal immunity in the absence of galectin-3

Galectin-3 (Gal-3) is the most studied member of the animal galectin family, which comprises β-galactoside-binding lectins and participates in several cellular events. Its expression in cells involved in innate and adaptive immunity is related to anti- and proinflammatory functions, signaling an important role in inflammatory, infectious, and tumorigenesis processes. Mice deficient in Gal-3 exhibit important phenotypes, but it is unclear whether these phenotypes reflect an impairment of the functions of this protein. Gal-3 plays an important role in modulating the immune response to different pathogenic microorganisms. However, the role of Gal-3 in immunity to infection is still poorly understood. Therefore, we investigated the effects of Gal-3 deletion on the expression of genes involved in the innate immune response in the lungs, spleens, and brains of Gal-3 KO mice. Gene profiling expression analysis suggested that Gal-3 deletion resulted in differentially modulated expression of the genes encoding beta-glucan, mannose and chitin-responsive pattern recognition receptors, signal transduction, inflammation, and phagocytosis. Our data thus suggest the importance of Gal-3 expression in the host innate immune system.

Medienart:

E-Artikel

Erscheinungsjahr:

2021

Erschienen:

2021

Enthalten in:

Zur Gesamtaufnahme - volume:12

Enthalten in:

Virulence - 12(2021), 1 vom: 04. Dez., Seite 981-988

Sprache:

Englisch

Beteiligte Personen:

Rezende, Caroline Patini [VerfasserIn]
Martins Oliveira Brito, Patricia Kellen [VerfasserIn]
Pessoni, Andre Moreira [VerfasserIn]
Da Silva, Thiago Aparecido [VerfasserIn]
Goldman, Gustavo H [VerfasserIn]
Almeida, Fausto [VerfasserIn]

Links:

Volltext

Themen:

Antifungal Agents
Antifungal immunity
Galectin 3
Galectin-3
Galectins
Gene expression
Gene knockout
Innate immune response
Journal Article
Research Support, Non-U.S. Gov't

Anmerkungen:

Date Completed 16.12.2021

Date Revised 16.12.2021

published: Print

Citation Status MEDLINE

doi:

10.1080/21505594.2021.1903212

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM323353401