IL17C (Interleukin 17C)

Additionally, organ-on-a-chip technology confirmed that SFALCA showed no significant toxicity to the liver. In conclusion, this study elucidates the active components and mechanisms of SFALCA in treating IBD and assesses its safety, providing a reliable in vitro platform for future therapeutic strategies.

Malignant ovarian neoplasms were associated with CCL20 and other markers. This study clarifies the causal relationships between circulating inflammatory markers and ovarian diseases, providing a crucial foundation for future translational research and clinical applications.

In addition, the role of IL-17C signaling in promoting endometriosis carcinogenesis was investigated by blocking and modulating the IL-17C/IL-17RE pathway in human endometriotic epithelial cells, endometrial organoids, and ovarian endometriosis mice. These data identified IL-17C signaling as a driver of endometriosis carcinogenesis and propose IL-17C/IL-17RE as promising therapeutic targets, particularly for EAOC cases characterized by high IL-17C expression.

Plasma inflammatory proteins causally influence DLBCL risk, partially mediated by metabolites. This underscores metabolite pathways as potential targets for therapeutic intervention.

IL-17C appears to play a protective role in some OSCC cells. While this study indicates the potential of using IL-17C as a therapeutic candidate for OSCC patients, its relatively mild and selective effect suggests it may be more effective as part of a combination therapy.

This study identifies a novel PPARγ/CEBPA/IL-17C/IL-17A signaling axis that promotes Th17 differentiation and contributes to tumor-associated inflammation in OSCC. Targeting PPARγ represents a promising strategy to inhibit tumor progression and modulate the immune microenvironment, providing new insight into immunotherapeutic approaches for OSCC.

Actinobacteria's protective effect appeared partially mediated through increased LIFR expression, accounting for 14% of the effect. Our findings suggest that modulating gut microbiota, particularly enhancing Actinobacteria, may serve as a novel strategy for VHD prevention and treatment.

In summary, this study identified significant causal relationships between six inflammatory proteins-Interleukin-17C, beta-nerve growth factor, C-C motif chemokine 20, Natural killer cell receptor 2B4, C-X-C motif chemokine 5, and Leukemia inhibitory factor-and CS risk through MR analysis. This finding not only emphasizes the important role of inflammation in the pathogenesis of CS but also suggests the potential value of inflammatory proteins as targets for early diagnosis and therapeutic interventions.

Four FDA-approved drugs-secukinumab (for ankylosing spondylitis, enthesitis-related arthritis, hidradenitis suppurativa, non-radiographic axial spondyloarthritis, plaque psoriasis, and psoriatic arthritis), ixekizumab (for ankylosing spondylitis, non-radiographic axial spondyloarthritis, plaque psoriasis, and psoriatic arthritis), brodalumab (for plaque psoriasis), and bimekizumab (for plaque psoriasis)-suppress the IL-17 pathway, with more in development, including netakimab, sonelokimab, izokibep, and CJM112. These agents and others are being studied across a spectrum of disorders. Understanding the complicated interplay between IL-17 and other immune mediators may yield new treatments for inflammatory/autoimmune conditions and malignancies.

P=N/A, N=56, Peking University Stomatological Hospital; Sunstar Co.Ltd

These results suggest that key inflammatory mediators could contribute to epileptogenesis and represent novel biomarkers and therapeutic targets in TSC.

There was a causal relationship between plasma lipidome and circulating inflammatory proteins with ED. Circulating inflammatory proteins appeared to mediate between triacylglycerol (56:3) levels and ED.