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The lineage stability and suppressive program of regulatory T cells require protein O-GlcNAcylation
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Journal Article
The lineage stability and suppressive program of regulatory T cells require protein O-GlcNAcylation
2019
Overview
Regulatory T (Treg) cells control self-tolerance, inflammatory responses and tissue homeostasis. In mature Treg cells, continued expression of FOXP3 maintains lineage identity, while T cell receptor (TCR) signaling and interleukin-2 (IL-2)/STAT5 activation support the suppressive effector function of Treg cells, but how these regulators synergize to control Treg cell homeostasis and function remains unclear. Here we show that TCR-activated posttranslational modification by O-linked N-Acetylglucosamine (O-GlcNAc) stabilizes FOXP3 and activates STAT5, thus integrating these critical signaling pathways. O-GlcNAc-deficient Treg cells develop normally but display modestly reduced FOXP3 expression, strongly impaired lineage stability and effector function, and ultimately fatal autoimmunity in mice. Moreover, deficiency in protein O-GlcNAcylation attenuates IL-2/STAT5 signaling, while overexpression of a constitutively active form of STAT5 partially ameliorates Treg cell dysfunction and systemic inflammation in O-GlcNAc deficient mice. Collectively, our data demonstrate that protein O-GlcNAcylation is essential for lineage stability and effector function in Treg cells.
The transcription factor Foxp3 and Stat5 modulate lineage stability and function of regulatory T (Treg) cells to promote immune homeostasis. Here the authors show that O-GlcNAcylation of Foxp3 and Stat5, mediated by O-GlcNAc transferase (OGT), is essential for Treg-mediate immune balance, with Treg-specific deficiency of OGT leading to severe autoimmunity.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14
/ 38
/ 38/91
/ 42/70
/ 64/60
/ 82/58
/ 96/95
/ Acetylglucosamine - immunology
/ Acetylglucosamine - metabolism
/ Animals
/ Female
/ Forkhead Transcription Factors - genetics
/ Forkhead Transcription Factors - immunology
/ Humanities and Social Sciences
/ Humans
/ Male
/ Mice
/ Protein Processing, Post-Translational
/ Proteins
/ Receptors, Antigen, T-Cell - genetics
/ Receptors, Antigen, T-Cell - immunology
/ Rodents
/ Science
/ STAT5 Transcription Factor - genetics
/ STAT5 Transcription Factor - immunology
