A5101457991- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Immune Cell Function and Interaction
- Neuroinflammation and Neurodegeneration Mechanisms
- Cytokine Signaling Pathways and Interactions
- Neurogenesis and neuroplasticity mechanisms
- Multiple Sclerosis Research Studies
- Psoriasis: Treatment and Pathogenesis
- Immune Response and Inflammation
- Systemic Lupus Erythematosus Research
- Immune cells in cancer
- Whipple's Disease and Interleukins
- Chemokine receptors and signaling
- Nerve injury and regeneration
- interferon and immune responses
- MicroRNA in disease regulation
- Retinoids in leukemia and cellular processes
- Circular RNAs in diseases
- Natural product bioactivities and synthesis
- Mesenchymal stem cell research
- Cell Adhesion Molecules Research
- Dermatology and Skin Diseases
- Bioactive natural compounds
- Cancer-related molecular mechanisms research
- RNA Interference and Gene Delivery
Thomas Jefferson University
2016-2025
Wuhu Fourth People Hospital
2025
Xian Yang Central Hospital
2025
Jefferson Hospital for Neuroscience
2004-2022
First Affiliated Hospital of Zhengzhou University
2011-2022
Guangzhou University of Chinese Medicine
2013-2021
Wannan Medical College
2016-2021
First Affiliated Hospital of Wannan Medical College
2016-2021
Shanxi Datong University
2012-2019
Hong Kong Baptist University
2015
Abstract Experimental autoimmune encephalomyelitis (EAE) serves as a model for multiple sclerosis and is considered CD4+, Th1 cell-mediated disease. IL-12 heterodimeric cytokine, composed of p40 p35 subunit, which thought to play an important role in the development cells can exacerbate EAE. We induced EAE with myelin oligodendrocyte glycoprotein (MOG) peptide 35–55 (MOG35–55) C57BL/6 mice found that while IL-12p40-deficient (−/−) are resistant EAE, IL-12p35−/− susceptible. Typical spinal...
Abstract IL-27 has been shown to play a suppressive role in experimental autoimmune encephalomyelitis (EAE) as demonstrated by more severe disease IL-27R-deficient (WSX-1−/−) mice. However, whether influences the induction or effector phase of EAE is unknown. This an important question therapies for diseases are generally started after autoreactive T cells have primed. In this study, we demonstrate maximal gene expression subunits and its receptor CNS at phases relapsing-remitting including...
Abstract IL-12 is thought to be involved in the susceptibility experimental autoimmune encephalomyelitis (EAE), a Th1 cell-mediated disorder of CNS. signals through heterodimeric receptor (IL-12Rβ1/IL-12Rβ2), whose β2-chain up-regulated on activated, autoreactive cells. Contrary expectation that absence IL-12Rβ2 would protect from EAE, we found IL-12Rβ2-deficient mice developed earlier and more severe disease, with extensive demyelination CNS inflammation. The inflammatory cells were mainly...
Abstract IL-17-producing CD8+ T cells (Tc17) appear to play a role in range of conditions, such as autoimmunity and cancer. Thus far, Tc17 have been only marginally studied, resulting paucity data on their biology function. We demonstrate that Th17 share similar developmental characteristics, including the previously unknown promoting effect IL-21 cell differentiation IL-23-dependent expression IL-22. Both STAT1 STAT4 are required for optimal development maximal secretion cytokines....
Adult neural stem cells (aNSCs) derived from the subventricular zone of brain show therapeutic effects in EAE, an animal model chronic inflammatory neurodegenerative disease MS; however, beneficial are modest. One critical weakness aNSC therapy may be insufficient antiinflammatory effect. Here, we demonstrate that i.v. or i.c.v. injection aNSCs engineered to secrete IL-10 (IL-10-aNSCs), a potent immunoregulatory cytokine, induced more profound functional and pathological recovery ongoing EAE...
Abstract Naturally occurring CD4+CD25+FOXP3+ regulatory T cells suppress the activity of pathogenic and prevent development autoimmune responses. There is growing evidence that TLRs are involved in modulating cell (Treg) functions both directly indirectly. Specifically, TLR2 stimulation has been shown to reduce suppressive function Tregs by mechanisms incompletely understood. The developmental pathways Th17 considered divergent mutually inhibitory, IL-17 secretion reported be associated with...
Multiple sclerosis (MS) is an autoimmune disease of the CNS. Studies in animal models MS have shown that GM-CSF produced by T cells necessary for development CNS inflammation. This suggests may a pathogenic role as well, and clinical trial testing its blockade ongoing. However, there been few reports on production MS. The objective this study was to characterize patients determine effect IFN-β therapy production. peripheral blood (PB) effects were characterized samples untreated...
Current multiple sclerosis (MS) medications are mainly immunomodulatory, having little or no effect on neuroregeneration of damaged central nervous system (CNS) tissue; they thus primarily effective at the acute stage disease, but much less so chronic stage. An MS therapy that has both immunomodulatory and neuroregenerative effects would be highly beneficial. Using in vivo vitro strategies, present study we demonstrate ursolic acid (UA), an antiinflammatory natural triterpenoid, also...
Abstract Here we design and optimize a genetically encoded fluorescent indicator, iAChSnFR, for the ubiquitous neurotransmitter acetylcholine, based on bacterial periplasmic binding protein. iAChSnFR shows large fluorescence changes, rapid rise decay kinetics, insensitivity to most cholinergic drugs. revealed transients in variety of slice vivo preparations mouse, fish, fly worm. will be useful study acetylcholine all animals.
Extracellular vesicles from oligodendrocytes restore antigen-specific immune tolerance in mice models of multiple sclerosis.
Abstract Dendritic cells (DCs) have been suggested to direct a type of Th differentiation through their cytokine profile, e.g., high IL-12/IL-23 for Th1 (named DC1/immunogenic DCs) and IL-10 Th2 (DC2/tolerogenic DCs). Suppressor signaling (SOCS)-3 is potent inhibitor Stat3 Stat4 transduction pathways IL-23 IL-12, respectively. We thus hypothesize that an enhanced SOCS-3 expression in DCs may block the autocrine response these cells, causing them become DC2-type phenotype will subsequently...
Abstract Experimental autoimmune encephalomyelitis is a well-characterized model of cell-mediated autoimmunity. TLRs expressed on APCs recognize microbial components and induce innate immune responses, leading to the elimination invading infectious agents. Certain TLR agonists have been reported adjuvant properties in CNS inflammatory demyelination. We report this study that TLR3 stimulation by polyinosinic-polycytidylic acid, double-stranded RNA analog, suppresses relapsing demyelination...
Abstract The central role of T cells in the induction immunological tolerance against i.v. Ags has been well documented. However, dendritic (DCs), most potent APCs, this process is not clear. In present study, we addressed issue by examining involvement two different DC subsets, CD11c+CD11b+ and CD11c+CD8+ DCs, tolerance. We found that mice injected with an autoantigen peptide myelin oligodendrocyte glycoprotein (MOG) developed less severe experimental autoimmune encephalomyelitis (EAE)...
Abstract IL-27 counters the effect of TGF-β+IL-6 on naive CD4+ T cells, resulting in near complete inhibition de novo Th17 development. In contrast, little is known about already differentiated cells. A better understanding how regulates these cells needed to evaluate therapeutic potential cells-associated diseases. this study, we show that had surprisingly committed despite its expression a functional IL-27R. Contrary differentiation did not suppress retinoid-related orphan receptor (ROR)γt...
Abstract Experimental autoimmune encephalomyelitis (EAE) is generally believed to be an disease of the central nervous system (CNS) caused by myelin‐specific Th1 and/or Th17 effector cells. The underlying cellular and molecular mechanisms, however, are not fully understood. Using mice deficient in IL‐9 (IL‐9 −/− ), we showed that plays a critical role EAE. Specifically, developed significantly less severe EAE than their WT counterparts following both immunization with myelin proteolipid...
The interleukin-17 (IL-17) cytokine family is crucial to the progression of experimental autoimmune encephalomyelitis (EAE), an animal model multiple sclerosis (MS). It has been shown in a neuroectoderm-specific knockout study that astrocyte-restricted ablation Act1, key and common transcription factor for signals mediated by IL-17 members (IL-17A, IL-17F, IL-17C), ameliorates EAE. However, effect Act1 deficiency astrocytes on ongoing disease, which clinical relevance MS therapy, not...
Natural compounds derived from medicinal plants have long been considered a rich source of novel therapeutic agents. Baicalin (Ba) is bioactive flavonoid compound the root Scutellaria baicalensis, an herb widely used in traditional medicine for treatment various inflammatory diseases. In this study, we investigate effects and mechanism action Ba experimental autoimmune encephalomyelitis (EAE), animal model multiple sclerosis (MS). effectively ameliorated clinical disease severity myelin...
Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide. Many microRNAs (miRNAs), small non-coding RNAs, are involved in regulating cell proliferation, metastasis, migration, invasion and apoptosis. We investigated expression miR-135a HCC lines clinical tissues. The effect on migration HepG2 MHCC-97L were examined using wound healing Transwell assay. determined miR-135a, forkhead box O1 (FOXO1), matrix metalloproteinase-2 (MMP-2) Snail real-time PCR western...
Abstract CD4+CD25hi FOXP3+ regulatory T cells (Tregs) maintain tolerance to self-Ags. Their defective function is involved in the pathogenesis of multiple sclerosis (MS), an inflammatory demyelinating disease CNS. However, mechanisms such are poorly understood. Recently, we reported that stimulation TLR2, which preferentially expressed by human Tregs, reduces their suppressive and skews them into a Th17-like phenotype. In this study, tested hypothesis TLR2 activation reduced Treg MS. We...