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encephalomyelitis/phosphatase
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Loss of Phosphatase and Tensin Homolog in APCs Impedes Th17-Mediated Autoimmune Encephalomyelitis.
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The PI3K signaling cascade in APCs has been recognized as an essential pathway to initiate, maintain, and resolve immune responses. In this study, we demonstrate that a cell type-specific loss of the PI3K antagonist phosphatase and tensin homolog (PTEN) in myeloid cells renders APCs toward a
Acid phosphatase activity in mouse brain infected with Venezuelan equine encephalomyelitis virus.
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The mode of development of Venezuelan equine encephalomyelitis virus and the activity of acid phosphatase in the central nervous system of newborn mice were investigated. Precursor particles appeared to be formed in masses of viroplasm, migrating to the membrane of the Golgi cisterns and vacuoles or
Resistance to experimental autoimmune encephalomyelitis and impaired T cell priming by dendritic cells in Src homology 2 domain-containing protein tyrosine phosphatase substrate-1 mutant mice.
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Src homology 2 domain-containing protein tyrosine phosphatase (SHP) substrate-1 (SHPS-1) is a transmembrane protein that binds the protein tyrosine phosphatases SHP-1 and SHP-2 through its cytoplasmic region and is expressed on the surface of CD11c(+) dendritic cells (DCs) and macrophages. In this
Critical role for protein tyrosine phosphatase SHP-1 in controlling infection of central nervous system glia and demyelination by Theiler's murine encephalomyelitis virus.
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We previously characterized the expression and function of the protein tyrosine phosphatase SHP-1 in the glia of the central nervous system (CNS). In the present study, we describe the role of SHP-1 in virus infection of glia and virus-induced demyelination in the CNS. For in vivo studies,
Expression of the tyrosine phosphatase SRC homology 2 domain-containing protein tyrosine phosphatase 1 determines T cell activation threshold and severity of experimental autoimmune encephalomyelitis.
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Experimental autoimmune encephalomyelitis (EAE) is a CD4 Th1-mediated inflammatory demyelinating disorder of the CNS and a well-established animal model for multiple sclerosis. Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1) is a cytosolic tyrosine phosphatase that is
Protein tyrosine phosphatase σ regulates autoimmune encephalomyelitis development.
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Protein tyrosine phosphatases (PTPs) play essential roles in regulating signaling events in multiple cells by tyrosine dephosphorylation. One of them, PTPσ, appears important in regulating function of plasmacytoid dendritic cells (pDC). Here we report that PTPσ deletion in knockout mice and
Ultracytochemical localization of alkaline phosphatase activity in endothelial cells in chronic relapsing experimental allergic encephalomyelitis.
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To investigate the functions of endothelial cells (ECs) in chronic relapsing experimental allergic encephalomyelitis (EAE), we examined ECs ultracytochemically in various stages of EAE, in conjunction with the localization of alkaline phosphatase (AP) activity. We also studied the relation between
MAP kinase phosphatase 2 deficient mice develop attenuated experimental autoimmune encephalomyelitis through regulating dendritic cells and T cells.
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Mitogen-activated protein kinase phosphatases (MKPs) play key roles in inflammation and immune mediated diseases. Here we investigated the mechanisms by which MKP-2 modulates central nervous system (CNS) inflammation in experimental autoimmune encephalomyelitis (EAE). Our results show that MKP-2
[The activity of proteolytic enzymes and acid phosphatase in nervous tissue at various states of the development of allergic encephalomyelitis].
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Phosphatases and phospholipases in the central nervous system. A study in normal states and in experimentally induced disseminated allergic encephalomyelitis.
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[Dynamics of changes in the non-specific phosphatases in the central nervous systems of white mice infected with the virus of acute human encephalomyelitis].
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ALKALINE PHOSPHATASE ISOENZYME SYSTEMS OF THE GUINEA PIG IN HEALTH AND IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS.
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Immunologic differences in murine glial cells and their association with susceptibility to experimental allergic encephalomyelitis.
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We tested the hypothesis that glial cells from mice resistant or susceptible to the autoimmune disease experimental allergic encephalomyelitis (EAE) may differ in their abilities either to express Ia antigens and/or stimulate anti-class II (Ia)-specific T-cells. Ia antigens were induced on glial
MiR-19b Functions as a Potential Protector in Experimental Autoimmune Encephalomyelitis.
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BACKGROUND
MicroRNA-19b (miR-19b) is essential in determining oligodendroglia proliferation. Phosphatase and tensin homologue on chromosome 10 (PTEN) is considered the target of miR-19b and participates in oligodendrocyte differentiation and proliferation.
METHODS
Murine EAE was induced by myelin
Endotoxin- and ATP-neutralizing activity of alkaline phosphatase as a strategy to limit neuroinflammation.
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BACKGROUND
Alkaline phosphatase (AP) is a ubiquitously expressed enzyme which can neutralize endotoxin as well as adenosine triphosphate (ATP), an endogenous danger signal released during brain injury. In this study we assessed a potential therapeutic role for AP in inhibiting neuroinflammation
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