Bingji Li

ORCID: 0000-0003-2419-7429
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About
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Research Areas
  • Peptidase Inhibition and Analysis
  • Cancer Research and Treatments
  • IL-33, ST2, and ILC Pathways
  • Ubiquitin and proteasome pathways
  • Cancer, Stress, Anesthesia, and Immune Response
  • Immune Cell Function and Interaction
  • Inflammation biomarkers and pathways
  • Dysphagia Assessment and Management
  • Mycobacterium research and diagnosis
  • Lung Cancer Research Studies
  • Immune cells in cancer
  • Protein Hydrolysis and Bioactive Peptides
  • Herbal Medicine Research Studies
  • Polyomavirus and related diseases
  • Contact Dermatitis and Allergies
  • Autoimmune and Inflammatory Disorders
  • Chemotherapy-induced organ toxicity mitigation
  • Inflammatory Bowel Disease
  • Aquatic life and conservation
  • Inflammasome and immune disorders
  • Electrolyte and hormonal disorders
  • Tracheal and airway disorders
  • Macrophage Migration Inhibitory Factor
  • Pediatric health and respiratory diseases
  • Immune Response and Inflammation

Fudan University
2015-2022

Shanghai Medical College of Fudan University
2013-2016

China Rehabilitation Research Center
2013

Abstract Cancer-associated fibroblasts (CAF) are components of the tumor microenvironment whose contributions to malignant progression not fully understood. Here, we show that fibroblast activation protein (FAP) triggers induction a CAF subset with an inflammatory phenotype directed by STAT3 and inflammation-associated expression signature marked CCL2 upregulation. Enforcing FAP in normal was sufficient endow them similar FAP+CAFs. We identified as persistent activator fibroblastic through...

10.1158/0008-5472.can-15-2973 article EN Cancer Research 2016-05-24

Chemerin is present in various inflammatory sites and closely involved tissue inflammation. Recent studies have demonstrated that chemerin treatment can cause either anti-inflammatory or pro-inflammatory effects according to the disease model being investigated. Elevated circulating was recently found patients with bowel (IBD); however, role of intestinal inflammation remains unknown. In this study, we administration exogenous (aa17–156) aggravated severity dextran sulfate sodium...

10.1038/cmi.2014.15 article EN cc-by-nc-sa Cellular and Molecular Immunology 2014-04-14

Desmoplasia is a hallmark of intrahepatic cholangiocarcinoma (ICC), which constitutes barrier to infiltration lymphocyte, but not myeloid cells. Given that dense desmoplastic stroma has been reported be We here investigated whether fibroblastic FAP influenced ICC progression via non-T cell-related immune mechanisms. demonstrated expression was critical for STAT3 activation and CCL2 production, ICC-CAFs were the primary source in human microenvironment by using ICC-Fbs from six patients....

10.1016/j.neo.2019.10.005 article EN cc-by-nc-nd Neoplasia 2019-11-20

Enhanced gut permeability due to dysregulated epithelial tight junction is often associated with inflammatory bowel diseases (IBD), which have a greater risk for developing colorectal cancer. STAT6 activation was detected in inflamed colonic epithelium of active IBD patients, suggesting role colitis development. Here, we demonstrated that non-hematopoietic STAT6, but not hematopoietic triggered DSS-induced and subsequent tumorigenesis. This could be the enhancing-effect on microbiota...

10.1038/s41385-019-0204-y article EN cc-by Mucosal Immunology 2019-09-18

Chemerin restricts cold-induced IL-33 production by beige adipocytes, impairing fat’s ability to dissipate excess energy stores.

10.1126/sciimmunol.abg9698 article EN Science Immunology 2021-07-29

Thymic stromal lymphopoietin (TSLP) has recently been suggested in several epithelial cancers, either pro-tumor or anti-tumor. However, the role of TSLP colon cancer remains unknown. We here found significantly decreased levels tumor tissues compared with tumor-surrounding patients and negatively correlated clinical staging score cancer. TSLPR, receptor TSLP, was expressed all three cell lines investigated tissues. The addition enhanced apoptosis cells a TSLPR-dependent manner....

10.18632/oncotarget.7614 article EN Oncotarget 2016-02-23

Intestinal barrier immunity is essential for controlling gut microbiota without eliciting harmful immune responses, while its defect contributes to the breakdown of intestinal homeostasis and colitis development. Chemerin, which abundantly expressed in tissues, has been demonstrated regulate tissue inflammation via CMKLR1, functional receptor. Several studies have reported association between increased expression chemerin–CMKLR1 disease severity immunotherapy resistance inflammatory bowel...

10.1073/pnas.2205574119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-07-11

Abstract The biochemical composition of six seahorse species from the Chinese coast was analyzed in this study. crude protein content (% dry weight) Hippocampus kuda , trimaculatus kelloggi spinosissimus histrix and comes 70.70 ± 2.12%, 77.59 1.06%, 78.31 1.74%, 71.15 1.32%, 68.07 1.96%, 76.59 3.25%, respectively. major amino acids (>5% total) seahorses were arginine, aspartic acid, glutamic alanine, glycine, there significant differences essential (EAA) (as % total protein) among ( P...

10.1111/j.1749-7345.2008.00159.x article EN Journal of the World Aquaculture Society 2008-03-31

Leukotriene B4 (LTB4 ) is a lipid mediator that rapidly generated in inflammatory sites, and its functional receptor, BLT1, mostly expressed on immune cells. Contact dermatitis common skin disease characterized by oedema abundant infiltrates, primarily including neutrophils CD8(+) T The role of the LTB4 -BLT1 axis contact remains largely unknown. In this study, we found up-regulated gene expression 5-lipoxygenase leukotriene A4 hydrolase, two critical enzymes for synthesis, BLT1 elevated...

10.1111/imm.12478 article EN Immunology 2015-05-09

Abstract Chemerin is characterized by a chemoattractant protein present in various inflammatory sites. Several studies have suggested that chemerin plays an anti-inflammatory role acute tissue inflammation inhibiting the recruitment of cells. It has been recently reported elevated patients with bowel disease (IBD), however, IBD remains unknown. In study, we examined for development DSS-induced experimental colitis. expression was up-regulated on days 5 and 8 after continuous DSS exposure...

10.4049/jimmunol.190.supp.136.19 article EN The Journal of Immunology 2013-05-01

<div>Abstract<p>Cancer-associated fibroblasts (CAF) are components of the tumor microenvironment whose contributions to malignant progression not fully understood. Here, we show that fibroblast activation protein (FAP) triggers induction a CAF subset with an inflammatory phenotype directed by STAT3 and inflammation-associated expression signature marked CCL2 upregulation. Enforcing FAP in normal was sufficient endow them similar FAP<sup>+</sup>CAFs. We identified as...

10.1158/0008-5472.c.6508205.v1 preprint EN 2023-03-31

<p>Supplemental Figures and Tables Figure S1. The purity of the isolated fibroblasts. S2. Knockdown FAP or STAT3 impairs inflammatory phenotype CAFs. S3. Forced expression in normal S4. uPAR has no effect on genes control S5. knockdown abolishes tumor-promoting effects CAFs Hepa1-6 tumor. S6. is dispensable for direct cancer stemness immune function MDSCs CD8+T cells. S7. Stromal p-STAT3 CCL2 negatively associated with survival ICC patients.</p>

10.1158/0008-5472.22411370.v1 preprint EN cc-by 2023-03-31

<p>Supplemental Figures and Tables Figure S1. The purity of the isolated fibroblasts. S2. Knockdown FAP or STAT3 impairs inflammatory phenotype CAFs. S3. Forced expression in normal S4. uPAR has no effect on genes control S5. knockdown abolishes tumor-promoting effects CAFs Hepa1-6 tumor. S6. is dispensable for direct cancer stemness immune function MDSCs CD8+T cells. S7. Stromal p-STAT3 CCL2 negatively associated with survival ICC patients.</p>

10.1158/0008-5472.22411370 preprint EN cc-by 2023-03-31

<div>Abstract<p>Cancer-associated fibroblasts (CAF) are components of the tumor microenvironment whose contributions to malignant progression not fully understood. Here, we show that fibroblast activation protein (FAP) triggers induction a CAF subset with an inflammatory phenotype directed by STAT3 and inflammation-associated expression signature marked CCL2 upregulation. Enforcing FAP in normal was sufficient endow them similar FAP<sup>+</sup>CAFs. We identified as...

10.1158/0008-5472.c.6508205 preprint EN 2023-03-31
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