A5078584153- NF-κB Signaling Pathways
- Psoriasis: Treatment and Pathogenesis
- Immune Response and Inflammation
- Immune Cell Function and Interaction
- IL-33, ST2, and ILC Pathways
- interferon and immune responses
- Inflammasome and immune disorders
- Whipple's Disease and Interleukins
- Cytokine Signaling Pathways and Interactions
- T-cell and B-cell Immunology
- Venomous Animal Envenomation and Studies
- Immune cells in cancer
- Antimicrobial Peptides and Activities
- Biochemical and Structural Characterization
- Cancer Immunotherapy and Biomarkers
- Ion channel regulation and function
- Enzyme Structure and Function
- Immunotherapy and Immune Responses
- Diabetes and associated disorders
- Fibroblast Growth Factor Research
- Systemic Lupus Erythematosus Research
- Dermatology and Skin Diseases
- Gut microbiota and health
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Immunodeficiency and Autoimmune Disorders
Shanghai Institute of Nutrition and Health
2018-2024
University of Chinese Academy of Sciences
2021-2024
ShanghaiTech University
2018-2024
Chinese Academy of Sciences
2011-2020
Shanghai Institutes for Biological Sciences
2011-2020
Shanghai Jiao Tong University
2011-2020
Center for Excellence in Molecular Cell Science
2017-2020
Shanghai Sixth People's Hospital
2020
Shanghai Eighth People Hospital
2019
Renji Hospital
2014-2016
Lung metastasis is the major cause of breast cancer-related mortality. The neutrophil-associated inflammatory microenvironment aids tumor cells in metastatic colonization lungs. Here, we show that tumor-secreted protease cathepsin C (CTSC) promotes breast-to-lung by regulating recruitment neutrophils and formation neutrophil extracellular traps (NETs). CTSC enzymatically activates membrane-bound proteinase 3 (PR3) to facilitate interleukin-1β (IL-1β) processing nuclear factor κB activation,...
Interleukin-1 (IL-1) receptor-associated kinase (IRAK) plays an important role in the sequential formation and activation of IL-1-induced signaling complexes. Previous studies showed that IRAK is recruited to IL-1-receptor complex, where it hyperphosphorylated. We now find phosphorylated turn recruits TRAF6 receptor complex (complex I), which differs from previous concept interacts with after leaves receptor. then brings TAK1, TAB1, TAB2, are preassociated on membrane before stimulation form...
The interleukin-1 (IL-1) receptor-associated kinase (IRAK) is required for the IL-1-induced activation of nuclear factor κB and c-Jun N-terminal kinase. goal this study was to understand how IRAK activates intermediate proteins TRAF6, TAK1, TAB1, TAB2. When phosphorylated in response IL-1, it binds membrane where forms a complex with TRAF6; TRAF6 then dissociates translocates cytosol. membrane-bound similarly mediates translocation TAB2 from Different regions are suggesting that each protein...
The Toll-interleukin-1 receptor (TIR) domain-containing orphan SIGIRR (single immunoglobulin interleukin-1 receptor-related protein) acts as a negative regulator of interleukin (IL)-1 and lipopolysaccharide (LPS) signaling. Endogenous transiently interacted with IL-1 the receptor-proximal signaling components (MyD88, IRAK, tumor necrosis factor receptor-associated 6) upon stimulation, indicating that interacts complex in ligand-dependent manner. Similar interaction was also observed between...
The adaptor protein Act1 functions as a ubiquitin ligase to mediate interleukin-17 receptor–dependent activation of nuclear factor-κB.
IL-17 is one of the most potent and actively investigated proinflammatory cytokines. In this study, we examined effect on mesenchymal stem cells (MSCs) under influence inflammatory Ironically, dramatically enhanced immunosuppressive MSCs induced by IFNγ TNFα, revealing a novel role in immunosuppression. Interestingly, found that action was dependent promoted expression key immune suppressive molecule, inducible nitric oxide synthase (iNOS), MSCs. concanavalin A (ConA)-induced hepatitis mouse...
Interleukin 17 (IL-17) plays critical roles in the pathogenesis of various autoimmune diseases, including experimental encephalomyelitis (EAE). How signals triggered by this powerful inflammatory cytokine are controlled to avoid abnormal responses is not well understood. In study, we report that TRAF3 a receptor proximal negative regulator IL-17 (IL-17R) signaling. greatly suppressed IL-17–induced NF-κB and mitogen-activated protein kinase activation subsequent production cytokines...
Although different autoimmune diseases show discrete clinical features, there are common molecular pathways intimately involved. Here we that miR-125a is downregulated in peripheral CD4+ T cells of human including systemic lupus erythematosus and Crohn’s disease, relevant mouse models. stabilizes both the commitment immunoregulatory capacity Treg cells. In miR-125a-deficient mice, balance appears to shift from immune suppression inflammation, results more severe pathogenesis colitis...
Abstract NOTCH1 signalling contributes to defective remyelination by impairing differentiation of oligodendrocyte progenitor cells (OPCs). Here we report that IL-17 stimulation induces activation in OPCs, contributing Th17-mediated demyelinating disease. Mechanistically, IL-17R interacts with via the extracellular domain, which facilitates cleavage NOTHC1 intracellular domain (NICD1). IL-17-induced results interaction adaptor Act1 NICD1, followed translocation Act1–NICD1 complex into...
ZBP1 senses viral Z-RNAs to induce necroptotic cell death restrain infection. is also thought recognize host cell-derived regulate organ development and tissue inflammation in mice. However, it remains unknown how the host-derived are formed these endogenous sensed by ZBP1. Here, we report that oxidative stress strongly induces Z-RNAs, then localize granules for direct sensing trigger necroptosis. Oxidative triggers dramatically increase Z-RNA levels tumor cells, directly necroptosis through...