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Article

A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance.

The Journal of experimental medicine - 2 Aug 2021

Warshauer Jeremy T, Belk Julia A, Chan Alice Y, Wang Jiaxi, Gupta Alexander R, Shi Quanming, Skartsis Nikolaos, Peng Yani, Phipps Jonah D, Acenas Dante, Smith Jennifer A, Tamaki Stanley J, Tang Qizhi, Gardner James M, Satpathy Ansuman T, Anderson Mark S

Abstract excerpt

Naturally occurring cases of monogenic type 1 diabetes (T1D) help establish direct mechanisms driving this complex autoimmune disease. A recently identified de novo germline gain-of-function (GOF) mutation in the transcriptional regulator STAT3 was found to cause neonatal T1D. We engineered a novel knock-in mouse incorporating this highly diabetogenic human STAT3 mutation (K392R) and found that these mice...

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Share to Autoimmunity
Share to CD8-Positive T-Lymphocytes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Cytotoxicity, Immunologic

Share to Diabetes Mellitus, Type 1

Share to Gain of Function Mutation

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Identifiers

PMID: 34115115
DOI: 10.1084/jem.20210759
PMCID: PMC8203485

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

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A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance.PMID 34115115Read ↗

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