The Crohn Disease-associated ATG16L1T300A polymorphism regulates inflammatory responses by modulating TLR- and NLR-mediated signaling

Ping Gao, Hongtao Liu, Huarong Huang, Yu Sun, Baoqian Jia, Baidong Hou, Xuyu Zhou, Warren Strober & Fuping Zhang
The mechanisms by which the ATG16L1T300A polymorphism affects cell function and causes an increased risk for the development of Crohn disease remain incompletely understood. Here we report that healthy individuals and mice bearing this polymorphism, even as heterozygotes, manifest enhanced TLR, and NLR cytokine and chemokine responses due to increased activation of NFKB. We elucidated the mechanism of the NFKB abnormality and found that in the ATG16L1T300A cell, there is enhanced polyubiquitination of TRAF6 or...
1 citation reported since publication in 2022.
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