Interaction between NKG2D and its ligands MICA/B activates the DAP12/SYK/p53/p21 axis to drive pulmonary fibrosis

This study proposes that the NKG2D-DAP12-SYK-p53-p21 axis may represent a novel pathogenic pathway in PF, potentially linking immune dysregulation to cellular senescence. Therapeutic targeting of NKG2D could thus hold promise for the concurrent modulation of immune-fibrotic crosstalk and fibrotic progression, which might offer a new strategic direction for PF management.

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Publication Details

Journal
Frontiers in Immunology
Published
2026-03-02
DOI
https://doi.org/10.3389/fimmu.2026.1770733
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Type
article
Field-Weighted Citation Impact
0.00
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article

Interaction between NKG2D and its ligands MICA/B activates the DAP12/SYK/p53/p21 axis to drive pulmonary fibrosis

Jinlian He, Qingming Ke, Ruimin Tian, Hong Ren et al.
Frontiers in Immunology
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
article

Interaction between NKG2D and its ligands MICA/B activates the DAP12/SYK/p53/p21 axis to drive pulmonary fibrosis

Jinlian He, Qingming Ke, Ruimin Tian, Hong Ren, Qiuzhu Chen, Hudan Pan, Caiping Zhao, Liang Liu
article en

Abstract

This study proposes that the NKG2D-DAP12-SYK-p53-p21 axis may represent a novel pathogenic pathway in PF, potentially linking immune dysregulation to cellular senescence. Therapeutic targeting of NKG2D could thus hold promise for the concurrent modulation of immune-fibrotic crosstalk and fibrotic progression, which might offer a new strategic direction for PF management.

Frontiers in ImmunologyVol. 17
Guangzhou University of Chinese Medicine (CN), Hennepin County (US), Guangzhou Experimental Station (CN)
Good health and well-being
Openalex Percentile: Top 36%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
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