IL18 (Interleukin 18)

Finally, our translational pathway should be prioritized with orthogonal confirmation, interference testing, and clinically meaningful reporting to be adopted in the field of laboratory medicine. This supports reproducible biomarkers for clinical decision-making.

The combination of KPT-8602 and IFN-γ can activate the pan-apoptotic pathway by upregulating ZBP1, thereby effectively inhibiting the growth of PCNSL. This study presented a promising new combination treatment strategy for PCNSL.

Mechanistically, NMN elevated kidney NAD+ levels and enhanced SIRT1 expression. These findings demonstrate that NMN protects against CIS-AKI by activating the NAD+-SIRT1 pathway, thereby reducing oxidative stress and inflammation, and suggest its potential as a therapeutic strategy for CIS-AKI.

Consistent with the in vivo results, the NF-κB/NLRP3 pathway and the secretion of inflammatory cytokines were inhibited after SNX10 knockdown in A549 cells. In summary, SNX10 downregulation mitigated sepsis-induced oxidative stress and pulmonary inflammation by inhibiting the NF-κB/NLRP3 pathway.

These findings indicate that serum miR-155 is significantly elevated in young lymphoma patients with serological evidence of active EBV infection and is statistically associated with inflammatory cytokines, particularly IL-32. miR-155 may represent a promising non-invasive biomarker reflecting EBV-related immune activation, although tissue-based EBV confirmation and mechanistic studies are required to establish causality.

On the other hand, depletion of DE Tfh cells via Ezh2 gene deletion, inhibition of EZH2 (using FDA-approved drug, tazemetostat), or anti-CXCR6 mAb led to tumor regression. These findings may be relevant to a subset of human AITL cases since we found that ~20-30% of AITL patient samples have concomitantly elevated expression of CXCR6, IL-18R1, and IFNG. Our study identified a pathogenic Tfh-like subset essential for AITL tumor progression in a mouse model and suggests that identifying and targeting a DE Tfh-like subset in AITL patients might be an effective strategy.

A novel pathway by which serum type-I IFN propagates innate immune dysfunction in SLE via the STAT1-STAT2/AIM2 inflammasome axis in monocytes has been revealed.

The anti-tumor immunity is abrogated by caspase-1 inhibitor VX-765, anti-IL-1β, and anti-IL-18...Finally, Tmem175-/- mice are more responsive to anti-PD-1. Our works implies TMEM175 to be a potential target for immunotherapy.

HO-1 showed a significant inverse correlation with HMGB-1 (r = -0.405, p = 0.001), KEAP1 was positively correlated with sST2 (r = 0.282, p = 0.029), and GPX4 was correlated with FGF21 (r = 0.255, p = 0.049); no other significant associations were found. β-thalassemia major patients exhibit significant endothelial and cardiac injury markers, altered lipid profiles, and selective upregulation of antioxidant and ferroptosis-related genes.

Furthermore, in muscle cells, MCC950 directly silences NLRP3 inflammasome signaling, inhibits pyroptosis and IL-1β/IL-18 secretion, suppresses muscle protein degradation to rescue cancer cachexia-driven muscle atrophy. These findings revealed the important role of NLRP3 inflammasome in cancer cachexia and also suggested the possibility of developing NLRP3 inflammasome inhibitors such as MCC950 to be novel therapeutic candidates for cancer cachexia treatment.

CDNPs robustly expanded T cells from patients whose products could not be manufactured using standard approaches, and these CDNP-derived CAR T cells controlled tumors in humanized mouse models. In a phase I trial of patients with CD19⁺ malignancies (NCT04684563), cGMP-compatible CDNPs enabled streamlined 3-day manufacturing of IL-18-expressing CD19 CAR T cells, yielding higher cell recovery and durable clinical responses without unexpected toxicities, supporting CDNPs as a platform for commercial CAR T cell production.

ILC1 from NV-HCC also displayed enhanced IL-2/IL-15 signaling and interactions with CD8 + T cells via HLA-E, suggestive of potential antitumor crosstalk. While our single-cell cohort size was limited, necessitating validation in larger datasets, our study reveals etiology-associated differences in ILC phenotypes in HCC and provides insight into their potential roles in modulating immune responses within the tumor microenvironment.