2026-05-22T00:46:58Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/66612024-09-27T08:11:12Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Saz-Leal, Paula
author
del Fresno, Carlos
author
Brandi, Paola
author
Martinez-Cano, Sarai
author
Dungan, Otto M.
author
Chisholm, John D.
author
Kerr, William G.
author
Sancho, David
funder
Ministerio de Economía y Competitividad (España)
funder
Ministerio de Economía, Industria y Competitividad (España)
funder
Asociación Española Contra el Cáncer
funder
Centro Nacional de Investigaciones Cardiovasculares Carlos III (España)
funder
Agencia Estatal de Investigación (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Comunidad de Madrid (España)
funder
Instituto de Salud Carlos III
funder
Fondation ACTERIA (Acting on European Research in Immunology and Allergology)
funder
Atresmedia
funder
Fundación La Marató TV3
funder
Unión Europea. Comisión Europea
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Fundación ProCNIC
2018-11-22T08:10:49Z
2018-11-22T08:10:49Z
2018
Cell Rep. 2018; 25(5):1118-1126
10.1016/j.celrep.2018.09.092
2211-1247
Cell Reports
30380404
http://hdl.handle.net/20.500.12105/6661
beta-Glucan-induced trained immunity in myeloid cells leads to long-term protection against secondary infections. Although previous studies have characterized this phenomenon, strategies to boost trained immunity remain undefined. We found that beta-glucan-trained macrophages from mice with a myeloid-specific deletion of the phosphatase SHIP-1 (LysM Delta SHIP-1) showed enhanced proinflammatory cytokine production in response to lipopolysaccharide. Following beta-glucan training, SHIP-1-deficient macrophages exhibited increased phosphorylation of Akt and mTOR targets, correlating with augmented glycolytic metabolism. Enhanced training in the absence of SHIP-1 relied on histone methylation and acetylation. Trained LysM Delta SHIP-1 mice produced increased amounts of proinflammatory cytokines upon rechallenge in vivo and were better protected against Candida albicans infection compared with control littermates. Pharmacological inhibition of SHIP-1 enhanced trained immunity against Candida infection in mouse macrophages and human peripheral blood mononuclear cells. Our data establish proof of concept for improvement of trained immunity and a strategy to achieve it by targeting SHIP-1.
eng
CANDIDA-ALBICANS INFECTION
IN-VIVO
INNATE IMMUNITY
MONOCYTES
PROTECTION
INFLAMMATION
REINFECTION
INDUCTION
VITRO
Targeting SHIP-1 in Myeloid Cells Enhances Trained Immunity and Boosts Response to Infection
journal article
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TargetingSHIP-1MyeloidCells_2018.pdf
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TargetingSHIP-1MyeloidCells_2018_suppl.pdf
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TargetingSHIP-1MyeloidCells_2018.pdf.txt
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TargetingSHIP-1MyeloidCells_2018_suppl.pdf.txt