IndraLab

Statements


ZRANB1 activates IL12. 6 / 6
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"Our data further suggested that Trabid mediated IL-12 and IL-23 induction plays an important role in mediating inflammatory T cell responses and the pathogenesis of EAE, an animal model of the autoimmune neuroinflammatory disease multiple sclerosis."

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"DC-conditional deletion of Trabid impairs IL-12 and IL-23 production in DCs and the generation of Th1 and Th17 subsets of inflammatory T cells, rendering mice refractory to the induction of EAE 180."

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"To elucidate the molecular mechanism by which Trabid mediates induction of IL-12 family of cytokines, we examined the role of Trabid in regulating TLR mediated activation of MAP kinases (MAPKs), IkappaB kinase (IKK) and downstream transcription factors known to regulate Il12 and Il23 gene induction XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"Conditional deletion of Zranb1 in dendritic cells impairs IL-12 and IL-23 production and the generation of T 1 and T 17 subsets of inflammatory T cells, rendering mice refractory to the induction of experimental autoimmune encephalomyelitis (EAE) ."

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"Conditional deletion of Zranb1 in dendritic cells impairs IL-12 and IL-23 production and the generation of T H 1 and T H 17 subsets of inflammatory T cells, rendering mice refractory to the induction of experimental autoimmune encephalomyelitis (EAE) 191 ."

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"Collectively, these results suggest that Trabid mediates induction of IL-12 and IL-23, thereby promoting T H 1 and T H 17 differentiation."