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Article

Deletion of IL-33R (ST2) abrogates resistance to EAE in BALB/C mice by enhancing polarization of APC to inflammatory phenotype.

PloS one - 1 Jan 2012

Milovanovic Marija, Volarevic Vladislav, Ljujic Biljana, Radosavljevic Gordana, Jovanovic Ivan, Arsenijevic Nebojsa, Lukic Miodrag L

Abstract excerpt

The administration of interleukin 33 and deletion of IL-33 receptor, ST2 molecule, affects the induction of autoimmunity in different experimental models of human autoimmune diseases. The aim of this study was to analyze the effect of ST2 deletion on the induction of experimental autoimmune encephalomyelitis (EAE) in resistant BALB/c mice. Mice were immunized with MOG(35-55) peptide or disease was induced by...

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Share to Dendritic Cells
Share to Encephalomyelitis, Autoimmune, Experimental

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interleukin-1 Receptor-Like 1 Protein

Share to Interleukin-33

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Source

Open in PubMed Open full text

Identifiers

PMID: 23028861
DOI: 10.1371/journal.pone.0045225
PMCID: PMC3445483

Genes

MOG
APC
TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Deletion of IL-33R (ST2) abrogates resistance to EAE in BALB/C mice by enhancing polarization of APC to inflammatory phenotype.PMID 23028861Read ↗

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