FOXP3 (Forkhead Box P3)

Through cellular and animal experiments, we demonstrate that P. micra promotes tumor growth by secreting p-cresol, a metabolite of amino acid fermentation, which elevates reactive oxygen species levels and induces FOXP3+ Treg differentiation, thereby fostering immunosuppression and tumor growth. Our study establishes a mechanistic link between intratumoral microbiota and the immune microenvironment, highlighting the microbial contribution to ESCC progression and prognosis.

We found multiple immune suppressive markers were enriched in the endosteum, including Foxp3, CD163, CD27, Pd-1, and Pd-l1, while proliferation markers were enriched in tumor cells in the marrow, including p38 Mapk, pan-Ras, Mek1, and phospho-Erk1/2. These findings shed light on the niche-specific proteins and pathways that are activated in breast cancer bone metastases and establish a user-friendly highly multiplexed approach for spatial proteomics in pre-clinical models of bone metastasis.

Our findings indicate that Grg3 confers protective effects in a murine model of imiquimod-induced psoriasis-like dermatitis. The potential therapeutic properties of Grg3 potentially involve modulation of NLRP3 inflammasome activation, suppression of NF-κB signaling, and restoration of Th17/Treg cell homeostasis.

Clinical parameters remain the dominant predictors of outcome in NSCLC, with immune cell densities providing only limited prognostic value for clinical stratification. The openly available code and datasets present a unique resource for method development or focused analysis.

Though results are not statistically significant and imprecise, serum FOXP3 and P16ink4A concentrations are likely associated with persistence and progression of cervical lesions. Their measurement may benefit the prognostic monitoring of cervical lesions.

MiR-200c restoration inhibits FOXP3 and suppresses metastatic progression in breast cancer. Targeting the miR-200c/FOXP3 axis presents a novel and promising therapeutic approach for advanced breast cancer.

TME as defined by CD8 and TP53 mutational status may have predictive value for success of ICI therapy for patients with NSCLC with EGFR mutations.

Pharmacokinetic-receptor occupancy (PK/RO) modeling showed that by masking wild-type IL2 in the periphery, WTX-124 produces high RO on TILs but low RO on peripheral lymphocytes, unlike non-alpha IL2s. These findings therefore identify the conditional activation of wild-type IL2 as a promising engineering strategy to improve IL2 tolerability without compromising its antitumor activity.

These results underscore the dynamic relationship between vascular architecture and immune infiltration in MTC, highlighting region-specific interactions that may influence tumor progression. The elevated D2-40+ density in metastatic cases and distinct immuno-vascular correlations suggest potential prognostic markers and therapeutic targets.

High PBK expression was associated with longer OS and RFS and remained an independent favorable prognostic factor in multivariate analysis. PBK expression in CRC is linked to proliferative tumor epithelial states, an immune-activated microenvironment, and favorable outcomes, supporting its utility as a prognostic biomarker.

These findings suggest that canine OMM exhibits immunological phenotypes analogous to those observed in human cancers. Taken together, the TIL profile holds significant potential as a prognostic biomarker for canine OMM treated with anti-PD-L1 antibody therapy.

We analyzed the T-ALL microenvironment from 40 T-ALL cases treated on the AALL0434 clinical trial and identified a subpopulation of bone-marrow-enriched CCR4+ FOXP3+ T-regulatory cells which express immune checkpoints (PD-1 and TIGIT) and could be targeted with anti-CCR4 therapy. Lastly, we describe the preclinical efficacy of an anti-CCR4 CAR-T in in vitro and in vivo models, paving the way for future translational efforts in chemotherapy refractory T-ALL.