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these findings show a feed-forward mechanism involving STAT4 and T-BET that modulates the outcome of IL-23 signaling in innate lymphoid cells
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IL-23 secreted by myeloid-derived suppressor cells (MDSCs) can activate the androgen receptor pathway in prostate tumour cells, promoting cell survival and proliferation in androgen-deprived conditions; results reveal that MDSCs promote castration-resistant prostate cancer by acting in a non-cell autonomous manner; treatments that block IL-23 can oppose MDSC-mediated resistance to castration in prostate cancer
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It has been shown in a genetic psoriasis model that N-WASP controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter.
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JunB has an essential role in IL-23-dependent pathogenicity of Th17 cells
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HO-1 enhanced STAT3 phosphorylation, which enriched to Il12b and Il23a loci and negatively regulated their transcription. These findings demonstrate the underlying mechanism through which a nutritional can interfere with the immune response. CUR silences IL-23/Th17-mediated pathology by enhancing HO-1/STAT3 interaction in dendritic cells.
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This study defines a critical IL-36/IL-23/IL-22 cytokine network instrumental for antimicrobial peptide production and host defense in intestinal mucosa damage using a mouse inflammatory bowel disease model.
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IL-23 drives differentiation of peripheral gamma-delta 17 T cells from adult bone marrow-derived precursors.
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In mice on a C57BL/6 background, neither IL-23p19 nor IL-17A plays a role for immune protection against L. major in the physiological context of natural infections.
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The hormone levels are significantly reduced and lymphocytic infiltration in the lacrimal gland in ovariectomized mice, whereas the frequency of Th17 cells in the blood and spleen and IL-17A and IL-23 expression in the lacrimal glands are increased, leading to reduced tear production and positive fluorescein staining in the cornea.
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this study unveiled the role of IL-23-dependent IL-17 induction in LdCen-/- parasite-induced immunity and subsequent protection against visceral leishmaniasis
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Results reveal the importance of the IL-23/IL-17 inflammatory axis in secondary brain injury after intracerebral hemorrhage.
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RIG-I expression is markedly increased in the affected skin derived from psoriasis patients and from both IL-23- and imiquimod -induced psoriasis-like mouse model.
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results show that IL-23 accounts for the main aspects of human and murine lupus including the expansion of double negative T cells, decreased IL-2, and increased IL-17 production
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this study shows that IL-23 but not IL-1 contributes to the IL-17A expression induced by subacute O3 exposure
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IL-23 released by keratinocytes in response to endogenous TLR4 ligands causes skin DCs, which selectively express IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD4(+) T cells that mediates epidermal thickening.
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In mice overexpressing IL23, enthesis-resident gamma/delta T cells accumulate in the enthesis, ciliary body, and aortic valve.
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we describe here a new IL-12 member IL-39 (IL-23p19/Ebi3) secreted by activated B cells that mediate inflammatory responses in lupus-like mice. Thus, IL-39 might contribute to immunopathogenic mechanisms of SLE.
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These data identify the important contributions of IL-23 to the development of elastase-induced pulmonary inflammation and emphysema.
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The inflammatory phenotype in barrier-defective skin is shaped by counterregulation between the TSLP/type 2 and IL-23/type 17 axes.
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IL-23 is another important bronchial epithelial cell-driven cytokine which may contribute to the development of house dust mite allergic sensitization and asthma.
