LITERATURE · PEER REVIEWED

ASH1L and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T-cell autoimmunity

Nature Communications · 2017 · Peer reviewed

COMPLETE CITATION

Citation and identifiers

Xia M, Liu J, Liu S, et al.. “ASH1L and lnc-Smad3 coordinate Smad3 locus accessibility to modulate iTreg polarization and T-cell autoimmunity.” Nature Communications. 8:15818 · doi:10.1038/ncomms15818.

PubMed ID
28598443

RESEARCH QUESTION

How do ASH1L and lnc-Smad3 regulate Smad3 locus accessibility during induced regulatory T-cell polarization and autoimmunity?

The immune-model study identifies an Ash1l-dependent chromatin mechanism in induced regulatory T cells but does not demonstrate an immune phenotype in heterozygous ASH1L-related disorder.

INTERPRETATION BOUNDARY

Read the finding and limit together.

What this study supports

Supports an Ash1l-dependent chromatin mechanism in induced regulatory T-cell polarization and autoimmunity models.

What it cannot establish

Immune model evidence does not establish an immune phenotype in heterozygous ASH1L-related disorder.

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