anti-Interleukin 1 Family Member 9 (IL1F9) Anticorps

Human Interleukin 1 Family Member 9 (IL1F9) interaction partners

1. this study not only advances our understanding of how IL-36 cytokines may control mucosal inflammation, but also establishes EGFR signaling as a potentially important modulator of IL-36 cytokine function

2. The expression of IL-36gamma by oral epithelial cells in response to P. gingivalis might enable the subsequent autocrine stimulation of PGLYRP2 expression. Our data identify how IL-36gamma may promote oral mucosal homeostasis by regulating PGLYRP2 expression.

3. Interleukin 36 gamma (IL-36gamma) is detected in the immune and vascular compartments in the tumor microenvironment.

4. serum IL-36gamma levels were higher in active systemic lupus erythematosus patients and correlated with disease activity and arthritis

5. Cathepsin S was identified as the major IL-36gamma-activating protease expressed in epithelial cells.

6. enhanced expression of IL-36gamma was observed in plasma and bronchoalveolar lavage fluid of patients with acute respiratory distress syndrome because of bacterial pneumonia

7. IL-36-mediated IL-6 and CXCL8 production in human lung fibroblasts and bronchial epithelial cells may be involved in pulmonary inflammation especially caused by bacterial or viral infections.

8. With a focus on the skin as a target for microbial and viral invasion, the current knowledge of IL-36: IL-36alpha, IL-36beta and IL-36gamma, functions is reviewed. One physiological function of the IL-36smay be to counteract microbial immune evasion. [Review]

9. IL-36gamma inhibits differentiation and induces inflammation of keratinocyte via Wnt signaling pathway in psoriasis.

10. IL-36gamma-stimulated endothelial cells secrete the proinflammatory chemokines IL-8, CCL2 and CCL20.

11. skin injury increases IL-36gamma via the activation of TLR3-SLUG-VDR axis and IL-36gamma induces REG3A to promote wound healing

12. Autocrine and Paracrine Regulation of Keratinocyte Proliferation through a Novel Nrf2-IL-36gamma Pathway

13. Here the authors show that Mycobacterium tuberculosis infection of macrophages induces IL-36gamma production in a 2-stage-regulated fashion.

14. IL-36gamma, a member of the IL-1 superfamily, is involved in host defense and contributes to proinflammatory responses and development of inflammatory diseases.

15. IL-36gamma is significantly more strongly expressed in the epidermis of patients with psoriasis-based erythroderma than in other inflammatory skin diseases.

16. Study shows that plasma concentrations of IL-36alpha and IL-36gamma are overexpressed in active systemic lupus erythematosus patients and that IL-36alpha has a substantial pro-inflammatory effect through regulation of IL-6 and CXCL8 production.

17. IRF6 is likely to promote inflammation to P. gingivalis through its regulation of IL-36gamma.

18. Findings indicate that Interleukin (IL)-1beta-induced interleukin 36 gamma (IL-36gamma) expression is mediated by the activation of transcriptional factors, NF-kappaB p65 and AP-1 (c-jun).

19. IL36G was identified as strong regulators of skin pathology in both lesional and non-lesional skin samples.

20. Decreased Langerhans cell responses to IL36G: altered innate immunity in patients with recurrent respiratory papillomatosis

Mouse (Murine) Interleukin 1 Family Member 9 (IL1F9) interaction partners

1. While Legionella pneumophila-induced mortality in IL-36alpha- or IL-36gamma-deficient mice was not different from that in wild-type animals, antibody-mediated neutralization of IL-36gamma in IL-36alpha(-/-) mice resulted in mortality similar to that observed in IL-36R(-/-) mice, indicating redundant and overlapping roles for these cytokines in experimental murine Legionella pneumophila pneumonia.

2. these data identify a critical role for IL-36gamma in immunity against influenza virus

3. results uncover an important role for IkappaBzeta in IL-36 signaling and validate IkappaBzeta as an attractive target for psoriasis therapy.

4. 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.

5. these findings reveal a fundamental contribution for the IL-36/IL-36R axis in regulating the Treg-Th9 cell balance with broad implications for Th cell-mediated disorders, such as inflammatory bowel diseases and particularly ulcerative colitis

6. skin injury increases IL-36gamma via the activation of TLR3-SLUG-VDR axis and IL-36gamma induces REG3A to promote wound healing

7. IL-36 promotes myeloid cell infiltration, activation, and inflammatory activity in skin

8. Data presented herein shed further light on involvement of T-bet in innate immunity and suggest that IL-36gamma, besides IFNgamma, may contribute to functions of this transcription factor in immunopathology.

9. Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36alpha, IL-36beta, and IL-36gamma) or antagonist (IL-36Ra) activity

10. A critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.