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Endothelial cell expression of a STING gain-of-function mutation initiates pulmonary lymphocytic infiltration
Journal article   Open access   Peer reviewed

Endothelial cell expression of a STING gain-of-function mutation initiates pulmonary lymphocytic infiltration

Kevin MingJie Gao, Kristy Chiang, Zhaozhao Jiang, Filiz T. Korkmaz, Harish P. Janardhan, Chinmay M. Trivedi, Lee J. Quinton, Sebastien Gingras, Katherine A. Fitzgerald and Ann Marshak-Rothstein
Cell reports (Cambridge), Vol.43(4), pp.114114-114114
04/23/2024
DOI: 10.1016/j.celrep.2024.114114
PMCID: PMC11108094
PMID: 38625791
url
https://doi.org/10.1016/j.celrep.2024.114114View
Published (Version of record) Open Access

Abstract

Patients afflicted with Stimulator of interferon gene (STING) gain -of -function mutations frequently present with debilitating interstitial lung disease (ILD) that is recapitulated in mice expressing the STING V154M mutation (VM). Prior radiation chimera studies revealed an unexpected and critical role for non-hematopoietic cells in initiating ILD. To identify STING -expressing non-hematopoietic cell types required for the development of ILD, we use a conditional knockin (CKI) model and direct expression of the VM allele to hematopoietic cells, fibroblasts, epithelial cells, or endothelial cells. Only endothelial cell -targeted VM expression results in enhanced recruitment of immune cells to the lung associated with elevated chemokine expression and the formation of bronchus -associated lymphoid tissue, as seen in the parental VM strain. These findings reveal the importance of endothelial cells as instigators of STING -driven lung disease and suggest that therapeutic targeting of STING inhibitors to endothelial cells could potentially mitigate inflammation in the lungs of STING -associated vasculopathy with onset in infancy (SAVI) patients or patients afflicted with other ILD-related disorders.
Cell Biology Life Sciences & Biomedicine Science & Technology

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