Jun Li

ORCID: 0000-0002-8653-3996
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About
Contact & Profiles
Research Areas
  • IL-33, ST2, and ILC Pathways
  • Eosinophilic Esophagitis
  • Immune Cell Function and Interaction
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Atherosclerosis and Cardiovascular Diseases
  • Psoriasis: Treatment and Pathogenesis
  • Dermatology and Skin Diseases
  • Cardiac Fibrosis and Remodeling
  • Neonatal Respiratory Health Research
  • Pregnancy-related medical research
  • Pharmacological Effects of Natural Compounds
  • Immune Response and Inflammation
  • Advanced Glycation End Products research
  • Autoimmune and Inflammatory Disorders Research

Peking University
2023

Peking University Third Hospital
2023

Huazhong University of Science and Technology
2018-2020

Hangzhou Hospital of Traditional Chinese Medicine
2019

Zhejiang Chinese Medical University
2019

Cincinnati Children's Hospital Medical Center
2019

University of Rostock
2015

Renji Hospital
2015

Shanghai Jiao Tong University
2015

University of Cincinnati
2014

Injury to the biliary epithelium triggers inflammation and fibrosis, which can result in severe liver diseases may progress malignancy. Development of a type 1 immune response has been linked injury pathogenesis; however, subset patients with atresia, most common childhood cholangiopathy, exhibit increased levels Th2-promoting cytokines. The relationship among different inflammatory drivers, epithelial repair, carcinogenesis remains unclear. Here, we determined that Th2-activating cytokine...

10.1172/jci73742 article EN Journal of Clinical Investigation 2014-06-01

Abstract Myocardial infarction ( MI ) is a major condition causing heart failure HF ). After , the renin angiotensin system RAS and its signalling octapeptide II (Ang II) interferes with cardiac injury/repair via AT 1 2 receptors 1R, 2R). Our study aimed at deciphering mechanisms underlying link between cellular components of immune response relying on rodent model as well patients. Flow cytometric analyses showed an increase in expression CD 4 + 2R cells rat spleen post‐infarction, but...

10.1111/jcmm.12574 article EN cc-by Journal of Cellular and Molecular Medicine 2015-05-20

IL-33 promotes type 2 immunity, epithelial repair, and tissue fibrosis by activating group innate lymphoid cells (ILC2). ILC2 lack all known surface markers of mature T, B, NK, myeloid cell lineages (Linneg), express the receptor ST2, release cytokines which contribute to cholangiocyte proliferation activation hepatic stellate cells. This pathway results in massive extrahepatic bile duct (EHBD) but also exacerbates liver fibrosis, suggesting that there may be tissue-specific subpopulations...

10.1371/journal.pone.0215481 article EN cc-by PLoS ONE 2019-04-25

Abstract The product of the Epstein-Barr virus-induced gene 3 (EBI3) associates with p28, an IL-12p35-related protein, to form IL-27. EBI3 also IL-12p35 a distinct heterodimer. function in innate as well adaptive immunity intracellular bacteria has not been established. Here we demonstrate that deficient mice exhibit reduced bacterial load following acute challenge Listeria monocytogenes or re-challenge animals previously immunized L. monocytogenes, suggesting plays negative role both and...

10.4049/jimmunol.178.supp.95.4 article EN The Journal of Immunology 2007-04-01
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