NDLI: Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.

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Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sriskantharajah, Srividya Ben-Addi, Abduelhakem Stockinger, Brigitta Kierdorf, Katrin Prinz, Marco Tsakiri, Niki Veldhoen, Marc Tsichlis, Philip N. Gückel, Eva Brender, Christine O'Garra, Anne Ley, Steven C. Kollias, George
Description	Author Affiliation: Sriskantharajah S ( Division of Immune Cell Biology, National Institute for Medical Research, London NW7 1AA, United Kingdom)
Abstract	Tumor progression locus 2 (TPL-2) expression is required for efficient polarization of naive T cells to Th1 effector cells in vitro, as well as for Th1-mediated immune responses. In the present study, we investigated the potential role of TPL-2 in Th17 cells. TPL-2 was found to be dispensable for Th17 cell differentiation in vitro, and for the initial priming of Th17 cells in experimental autoimmune encephalomyelitis (EAE), a Th17 cell-mediated disease model for multiple sclerosis. Nevertheless, TPL-2-deficient mice were protected from EAE, which correlated with reduced immune cell infiltration, demyelination, and axonal damage in the CNS. Adoptive transfer experiments demonstrated that there was no T cell-intrinsic function for TPL-2 in EAE, and that TPL-2 signaling was not required in radiation-sensitive hematopoietic cells. Rather, TPL-2 signaling in radiation-resistant stromal cells promoted the effector phase of the disease. Importantly, using a newly generated mouse strain expressing a kinase-inactive form of TPL-2, we demonstrated that stimulation of EAE was dependent on the catalytic activity of TPL-2 and not its adaptor function to stabilize the associated ubiquitin-binding protein ABIN-2. Our data therefore raise the possibility that small molecule inhibitors of TPL-2 may be beneficial in multiple sclerosis therapy.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300172
Journal	The Journal of Immunology
Issue Number	8
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-04-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Encephalomyelitis, Autoimmune, Experimental Genetics Gene Expression Regulation Map Kinase Kinase Kinases Proto-oncogene Proteins Animals Astrocytes Immunology Metabolism Cell Differentiation Cytokines Chemically Induced Enzyme Activation Lymphocyte Activation Mice Mice, Transgenic Microglia Myelin-oligodendrocyte Glycoprotein Adverse Effects Peptide Fragments Signal Transduction T-lymphocyte Subsets Th17 Cells Cytology Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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B cells promote induction of experimental autoimmune encephalomyelitis by facilitating reactivation of T cells in the central nervous system.

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Suppression of inflammatory responses during myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis is regulated by AKT3 signaling.

Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

Fasudil regulates T cell responses through polarization of BV-2 cells in mice experimental autoimmune encephalomyelitis.

IFN-ß treatment requires B cells for efficacy in neuroautoimmunity.

HLA class II transgenic mice authenticate restriction of myelin oligodendrocyte glycoprotein‐specific immune response implicated in multiple sclerosis pathogenesis

Exploring the roles of CD8+ T lymphocytes in the pathogenesis of autoimmune demyelination

Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.

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Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.