transforming-growth-factor-beta and Encephalomyelitis

transforming-growth-factor-beta has been researched along with Encephalomyelitis* in 5 studies

Reviews

1 review(s) available for transforming-growth-factor-beta and Encephalomyelitis

ArticleYear
Th17 Cells and autoimmune encephalomyelitis (EAE/MS).
    Allergology international : official journal of the Japanese Society of Allergology, 2008, Volume: 57, Issue:2

    Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune disease affecting the central nervous system. It was largely accepted that Th1 cells driven by IL-12 were pathogenic T cells in human MS and experimental autoimmune encephalomyelitis, an animal model of MS. Recent data have established that IL-17-producing CD4+ T cells, driven by IL-23 and referred to as Th17 cells, play a pivotal role in the pathogenesis of EAE. A combination of TGF-beta and IL-6 induce Th17 cell lineage commitment via expression of transcription factor RORgammat. Th17 cells and induced Foxp3+ T regulatory cells are in reciprocal position in the T cell lineage commitment governed by TGF-beta and IL-6. The vitamin A metabolite retinoic acid is involved in this process via TGF-beta dependent induction of Foxp3. We have demonstrated that human Th17 cells could be identified as CCR2+ CCR5- memory CD4+ T cells. It is becoming clear that IL-23/Th17 axis also plays an important role in the pathogenesis of various human autoimmune diseases including MS. Additionally, accumulating evidences raise a possibility that CCR2 on Th17 cells may be a therapeutic target in MS.

    Topics: Animals; Autoimmune Diseases; Cell Differentiation; Encephalomyelitis; Encephalomyelitis, Autoimmune, Experimental; Forkhead Transcription Factors; Humans; Interleukins; Multiple Sclerosis; Nuclear Receptor Subfamily 1, Group F, Member 3; Receptors, CCR2; Receptors, Retinoic Acid; Receptors, Thyroid Hormone; T-Lymphocyte Subsets; T-Lymphocytes, Helper-Inducer; Th1 Cells; Transforming Growth Factor beta

2008

Other Studies

4 other study(ies) available for transforming-growth-factor-beta and Encephalomyelitis

ArticleYear
Effect of IL-10 Deficiency on TGFβ Expression during Fatal Alphavirus Encephalomyelitis in C57Bl/6 Mice.
    Viruses, 2022, 08-16, Volume: 14, Issue:8

    Sindbis virus (SINV) causes viral encephalitis in mice with strain-dependent virulence. Fatal encephalomyelitis in C57Bl/6 mice infected with a neuroadapted strain of SINV (NSV) is an immunopathogenic process that involves Th17 cells modulated by the regulatory cytokine IL-10. To further characterize the pathogenic immune response to NSV, we analyzed the regulation of transforming growth factor (TGF)-b in both wild-type (WT) and IL-10-deficient mice. NSV infection upregulated the expression of TGFb1 and TGFb3 in the central nervous system (CNS). In the absence of IL-10, levels of brain

    Topics: Alphavirus Infections; Animals; Encephalomyelitis; Immunity, Innate; Interleukin-10; Mice; Mice, Inbred C57BL; RNA, Messenger; Sindbis Virus; Th17 Cells; Transforming Growth Factor beta

2022
Smad7 in intestinal CD4
    Proceedings of the National Academy of Sciences of the United States of America, 2019, 12-17, Volume: 116, Issue:51

    Environmental triggers acting at the intestinal barrier are thought to contribute to the initiation of autoimmune disorders. The transforming growth factor beta inhibitor Smad7 determines the phenotype of CD4

    Topics: Animals; Autoimmunity; CD4-Positive T-Lymphocytes; Cell Differentiation; Central Nervous System; Disease Models, Animal; Encephalomyelitis; Encephalomyelitis, Autoimmune, Experimental; Gastrointestinal Microbiome; Gene Expression Regulation; Humans; Immune Tolerance; Inflammation; Intestines; Mice; Mice, Transgenic; Multiple Sclerosis; Signal Transduction; Smad7 Protein; Spinal Cord; Transforming Growth Factor beta

2019
Smad2 positively regulates the generation of Th17 cells.
    The Journal of biological chemistry, 2010, Sep-17, Volume: 285, Issue:38

    Development of Foxp3(+) regulatory T cells and pro-inflammatory Th17 cells from naive CD4(+) T cells requires transforming growth factor-β (TGF-β) signaling. Although Smad4 and Smad3 have been previously shown to regulate Treg cell induction by TGF-β, they are not required in the development of Th17 cells. Thus, how TGF-β regulates Th17 cell differentiation remains unclear. In this study, we found that TGF-β-induced Foxp3 expression was significantly reduced in the absence of Smad2. More importantly, Smad2 deficiency led to reduced Th17 differentiation in vitro and in vivo. In the experimental autoimmune encephalomyelitis model, Smad2 deficiency in T cells significantly ameliorated disease severity and reduced generation of Th17 cells. Furthermore, we found that Smad2 associated with retinoid acid receptor-related orphan receptor-γt (RORγt) and enhanced RORγt-induced Th17 cell generation. These results demonstrate that Smad2 positively regulates the generation of inflammatory Th17 cells.

    Topics: Animals; Cell Differentiation; Cell Line; Cells, Cultured; Disease Models, Animal; Encephalomyelitis; Forkhead Transcription Factors; Gene Expression; Humans; Immunoprecipitation; Interleukin-17; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Orphan Nuclear Receptors; Protein Binding; Reverse Transcriptase Polymerase Chain Reaction; Smad2 Protein; T-Lymphocytes; T-Lymphocytes, Helper-Inducer; Transforming Growth Factor beta

2010
Delivery to the central nervous system of a nonreplicative herpes simplex type 1 vector engineered with the interleukin 4 gene protects rhesus monkeys from hyperacute autoimmune encephalomyelitis.
    Human gene therapy, 2001, May-20, Volume: 12, Issue:8

    Systemic administration of antiinflammatory molecules to patients affected by immune-mediated inflammatory demyelinating diseases of the central nervous system (CNS) has limited therapeutic efficacy due to the presence of the blood-brain barrier (BBB). We found that three of five rhesus monkeys injected intrathecally with a replication-defective herpes simplex virus (HSV) type 1-derived vector engineered with the human interleukin 4 (IL-4) gene were protected from an hyperacute and lethal form of experimental autoimmune encephalomyelitis induced by whole myelin. The intrathecally injected vector consistently diffused within the CNS via the cerebrospinal fluid and infected ependymal cells, which in turn sustained in situ production of IL-4 without overt immunological or toxic side effects. In EAE-protected monkeys, IL-4-gene therapy significantly decreased the number of brain as well as spinal cord inflammatory perivenular infiltrates and the extent of demyelination, necrosis, and axonal loss. The protective effect was associated with in situ downregulation of inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein 1 (MCP-1), upregulation of transforming growth factor beta (TGF-beta), and preservation of BBB integrity. Our results indicate that intrathecal delivery of HSV-1-derived vectors containing antiinflammatory cytokine genes may play a major role in the future therapeutic armamentarium of inflammatory CNS-confined demyelinating diseases and, in particular, in the most fulminant forms where conventional therapeutic approaches have, so far, failed to achieve a satisfactory control of the disease evolution.

    Topics: Animals; Autoimmune Diseases; Blood-Brain Barrier; Brain; Cell Division; Central Nervous System; Chemokine CCL2; Cytokines; Down-Regulation; Encephalomyelitis; Enzyme-Linked Immunosorbent Assay; Genetic Therapy; Genetic Vectors; Herpesvirus 1, Human; Humans; Interleukin-4; Macaca mulatta; Magnetic Resonance Imaging; Male; Reverse Transcriptase Polymerase Chain Reaction; Spinal Cord; T-Lymphocytes; Time Factors; Transforming Growth Factor beta; Tumor Necrosis Factor-alpha; Up-Regulation

2001
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