Reduced Expression of miR-23a Suppresses A20 in TLR-stimulated Macrophages

Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease

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MicroRNA-93 inhibits inflammatory cytokine production in LPS-stimulated murine macrophages by targeting IRAK4

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All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity

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The TGF-β-inducible miR-23a cluster attenuates IFN-γ levels and antigen-specific cytotoxicity in human CD8+ T cells

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Autocrine and paracrine modulation of microRNA-155 expression by globular adiponectin in RAW 264.7 macrophages: Involvement of MAPK/NF-κB pathway

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A20-mediated negative regulation of canonical NF-κB signaling pathway

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A20 in inflammation and autoimmunity

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Involvement of A20 in the molecular switch that activates the non-canonical NF-кB pathway

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miR-486 sustains NF-κB activity by disrupting multiple NF-κB-negative feedback loops

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The NF-κB member p65 controls glutamine metabolism through miR-23a

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A miR-19 regulon that controls NF-κB signaling

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MicroRNAs miR-125a and miR-125b constitutively activate the NF- B pathway by targeting the tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20)

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Pathogen Recognition by the Innate Immune System

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MicroRNAs in inflammation and immune responses

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Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk

(2011) Xingguang Liu et al.   NATURE IMMUNOLOGY

MicroRNAs are expressed and processed by human primary macrophages

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TLR-signaling Networks

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Inhibition of NF- B Signaling by A20 Through Disruption of Ubiquitin Enzyme Complexes

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Regulation of Adaptive Immunity by the Innate Immune System

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Isolation of Mouse Peritoneal Cavity Cells

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