Interleukin 23 Proteins (IL23)

Mouse (Murine) Interleukin 23 (IL23) interaction partners

1. Our study demonstrates that in dendritic cells infected with Lymphocytic choriomeningitis virus, TLR activation with bacterial PAMPs resulted in reduced IL-12 and IL-23 expression compared to non-infected cells.

2. Blocking the IL-23 cytokine activity decreased liver cancer development in murine model.

3. Our work uncovers the IL-23-IL-22 signaling as a regulator of atherosclerosis that restrains expansion of pro-atherogenic microbiota and argues for informed use of cytokine blockers to avoid cardiovascular side effects driven by microbiota and inflammation.

4. IL-23p19 is a key cytokine responsible for induction of Leishmania-specific Th17 cells that play an important role for progressive disease in susceptible BALB/c mice

5. these findings show a feed-forward mechanism involving STAT4 and T-BET that modulates the outcome of IL-23 signaling in innate lymphoid cells

6. 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

7. 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.

8. JunB has an essential role in IL-23-dependent pathogenicity of Th17 cells

9. 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.

10. 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.

11. IL-23 drives differentiation of peripheral gamma-delta 17 T cells from adult bone marrow-derived precursors.

12. 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.

13. 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.

14. this study unveiled the role of IL-23-dependent IL-17 induction in LdCen-/- parasite-induced immunity and subsequent protection against visceral leishmaniasis

15. Results reveal the importance of the IL-23/IL-17 inflammatory axis in secondary brain injury after intracerebral hemorrhage.

16. 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.

17. 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

18. this study shows that IL-23 but not IL-1 contributes to the IL-17A expression induced by subacute O3 exposure

19. 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.

20. In mice overexpressing IL23, enthesis-resident gamma/delta T cells accumulate in the enthesis, ciliary body, and aortic valve.

Pig (Porcine) Interleukin 23 (IL23) interaction partners

1. These results provide genetic information about both swine IL-23 the IL-23 receptor alpha (IL-23Ralpha) and IL-12 receptor beta1 (IL-12Rbeta1), which allows for better understanding of interleukin systems involved in pig immunity.