anti-Interleukin 1 Family Member 9 (IL1F9) Anticorps

Human Interleukin 1 Family Member 9 (IL1F9) interaction partners

1. data indicate that IL-36gamma may participate as a key player in host defense mechanisms against invading pathogens in the female reproductive tract.

2. The results presented here confirm that IL-36gamma is a robust, specific, and reliable biomarker for psoriatic inflammation that outperforms previously reported biomarkers and is likely to withstand all challenges in real-life primary and secondary dermatologic care.

3. Polymorphisms in IL36G gene are associated with plaque psoriasis. IL36G has previously demonstrated markedly increased levels in plaque psoriasis patients and is linked to IL-23/IL-17 axis critical in psoriasis pathology.

4. Increased production and activation of IL-36gamma may act on neutrophils and further exaggerate neutrophilic inflammation in CRS.

5. 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

6. 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.

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

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

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

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

11. 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.

12. 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]

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

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

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

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

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

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

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

20. 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.

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

1. data indicate that IL-36gamma may participate as a key player in host defense mechanisms against invading pathogens in the female reproductive tract.

2. 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.

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

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

5. 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.

6. 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

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

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

9. 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.

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

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