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. 2022 Feb;15(2):195-197.
doi: 10.1038/s41385-022-00486-y. Epub 2022 Feb 23.

The LIGHT switch: mechanisms of fibroblast pathology in eosinophilic esophagitis

Zoe M X Chua  1 , Anne L Fletcher  2   3
Affiliations

The LIGHT switch: mechanisms of fibroblast pathology in eosinophilic esophagitis

Zoe M X Chua et al. Mucosal Immunol. 2022 Feb.
No abstract available

PubMed Disclaimer

Conflict of interest statement

A.L.F. is a scientific advisory board member and engaged in a collaborative research agreement with Phenomic A.I.

Figures

Fig. 1
Fig. 1. LIGHT-driven fibroblast differentiation.
LIGHT imposes a pro-inflammatory phenotype on esophageal fibroblasts by signaling through HVEM or LTβR. LIGHT-HVEM signaling is proposed to activate the canonical NFkB pathway. In the canonical signaling pathway, adaptor proteins are recruited to form the IKK complex, which degrades the IκB inhibitor, leading to nuclear translocation of NF-kB dimers and gene transcription. In contrast, LIGHT-LTβR signaling is thought to mainly occur via the non-canonical NF-kB pathway. In the non-canonical pathway, ligand binding drives NIK to activate IKKα, which phosphorylates the p100 molecule that is then cleaved to produce p52, which translocates into the nucleus as a heterodimer with RelB, where it promotes pro-inflammatory and anti-homeostatic gene expression. Together, these pathways play a primary role in driving homeostatic fibroblasts towards pathogenic pro-inflammatory fibroblasts in eosinophilic esophagitis.
See this image and copyright information in PMC

References

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