A5092232978- Peptidase Inhibition and Analysis
- Immune Cell Function and Interaction
- Nuclear Physics and Applications
- Drug Transport and Resistance Mechanisms
- Cancer Immunotherapy and Biomarkers
- CAR-T cell therapy research
- Radiation Therapy and Dosimetry
- Blood groups and transfusion
- Signaling Pathways in Disease
- Diabetes and associated disorders
- Boron Compounds in Chemistry
- Complement system in diseases
- Nanoplatforms for cancer theranostics
- Protein Degradation and Inhibitors
- Adenosine and Purinergic Signaling
- Immune Response and Inflammation
Center for Life Sciences
2025
State Key Laboratory of Membrane Biology
2025
Tsinghua University
2025
Wenzhou Medical University
2025
Qilu Hospital of Shandong University
2023-2025
Union Hospital
2024
Huazhong University of Science and Technology
2024
Cyclic GMP-AMP synthase (cGAS), a critical cytosolic DNA sensor initiating innate immune responses in the presence of DNA, is increasingly recognized as promising therapeutic target for ulcerative colitis (UC). Here, we reported design, synthesis, structure-activity relationship exploration and biological evaluation novel class CRBN-recruiting cGAS-targeting PROTAC degraders. Among them, TH35 exhibited most favorable degradation profile, achieving potent selective cGAS, markedly attenuated...
Sepsis is a critical global health concern linked to high mortality rates, often due acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). While the gut-lung axis involvement in ALI recognized, direct migration of gut immune cells remains unclear. Our study reveals sepsis-induced γδ T17 from small intestine lung, triggering an IL-17A-dominated inflammatory response mice. Wnt signaling activation alveolar macrophages drives CCL1 upregulation, facilitating cell migration. CD44
<title>Abstract</title> Sepsis is a severe global health issue with high mortality rates, and sepsis-associated encephalopathy (SAE) further exacerbates this risk. While recent studies have shown the migration of gut immune cells to lungs after sepsis, their impact on central nervous system remains unclear. Our research demonstrates that sepsis could induce IL-7R<sup>high</sup> CD8<sup>low</sup> γδ T17 from small intestine meninges, where they secrete IL-17A, impairing mitochondrial function...