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http://purl.uniprot.org/citations/35967337http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35967337http://www.w3.org/2000/01/rdf-schema#comment"

Background

Atopic dermatitis (AD), a common type 2 inflammatory disease, is driven by T helper (TH) 2/TH22polarization and cytokines.Galectin-9 (Gal-9), via its receptor T cell immunoglobulin- and mucin-domain-containing molecule-3 (TIM-3), can promote TH2/TH22 immunity. The relevance of this in AD is largely unclear.

Objectives

To characterize the role of TIM-3 and Gal-9 in the pathogenesis of AD and underlying mechanisms.

Methods

We assessed the expression of Gal-9 and TIM-3 in 30 AD patients, to compare them with those of 30 healthy controls (HC) and to explore possible links with disease features including AD activity (SCORAD), IgE levels, and circulating eosinophils and B cells. We also determined the effects of Gal-9 on T cells from the AD patients.

Results

Our AD patients had markedly higher levels of serum Gal-9 and circulating TIM-3-expressing TH1 and TH17 cells than HC. Gal-9 and TIM-3 were linked to high disease activity, IgE levels, and circulating eosinophils and/or B cells. The rates of circulating TIM-3-positive CD4+ cells were positively correlated with rates of TH2/TH22 cells and negatively correlated with rates of TH1/TH17 cells. Gal-9 inhibited the proliferation and induced the apoptosis of T cells in patients with AD, especially in those with severe AD.

Conclusion

Our findings suggest thatGal-9, via TIM-3, contributes to the pathogenesis of AD by augmenting TH2/TH22 polarization through the downregulation of TH1/TH17immunity. This makes Gal-9 and TIM-3 interesting to explore further, as possible drivers of disease and targets of novel AD treatment."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2022.952338"xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Ji J."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Liu C."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Shen Y."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Yang S."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Tang M."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Su W."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Maurer M."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/author"Jiao Q."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/name"Front Immunol"xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/pages"952338"xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/title"Galectin-9 contributes to the pathogenesis of atopic dermatitis via T cell immunoglobulin mucin-3."xsd:string
http://purl.uniprot.org/citations/35967337http://purl.uniprot.org/core/volume"13"xsd:string
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