IL2RA expression

In multivariate analysis, higher PB blast percentage, CD25 positivity, and ECOG PS ≥ 2 independently predicted poorer OS. Although LA did not reduce early mortality in the entire cohort, the loss of prognostic significance of elevated LDH, high PB blast percentage, PB monocyte burden, and CD25 expression in the LA group may suggest that the intervention can attenuate the impact of biologically aggressive disease.

In addition, combined treatment with BPA and 5-fluorouracil (5-FU), a commonly used chemotherapeutic agent for CRC, notably enhanced the anti-tumor effect in mice. These findings indicate that BPA, an active extract of B. pilosa L., showed antitumor activity in mice by suppressing the differentiation of pro-tumorigenic TAMs and Tregs within the TME.

AML with KMT2A-PTD shows distinctive immunophenotypic features with increased CD123 and aberrant CD25 expression, both associated with FLT3-ITD. These markers may have diagnostic and therapeutic relevance in this AML subtype.

Overall, the IL-12 release substantially improved effector functionality against CD176+ cells but not CD176- cells, indicating efficacy while maintaining specificity. Thus, CD176-iIL12-TRUCKs, with their potent antitumor efficacy and TME modulation potential, are a promising treatment option for patients with a variety of advanced solid tumors.

In orthotopic tumor models, mimicking systemic loss of Il27ra significantly reduced tumor growth and prolonged survival in immunocompetent mice, with single-cell profiling indicating enhanced intratumoral T-cell and NK-cell effector activity. Collectively, our findings identify an epithelial-intrinsic IL27RA-PI3K/AKT-MHC-I axis as a central driver of immune evasion and ICB resistance in TNBC and support IL27RA as a promising therapeutic target for overcoming immunotherapy resistance.

In summary, exosomal PA28γ induces a T-cell exhaustion phenotype by inhibiting their tumor-killing ability, promoting malignant progression via the PA28γ/BCLAF1/CD25&LAG-3 pathway. These findings reveal a novel cell‒cell interaction between tumors and T cells in the HNSCC microenvironment.

This activation was specifically abolished by ICOSL blockade, establishing the functional significance of this pathway. Our findings provide novel insights into tumor-immune interactions in cholangiocarcinoma and suggest the ICOS-ICOSL axis as a potential therapeutic target for immunotherapy.

We confirmed that SABR stimulates the immune system, which impacts patient clinical outcomes. A simultaneous increase in the percentage of PD-1+ lymphocytes and upregulation of Th17 response after SABR is an independent favorable prognostic factor.

The kit can be stored at -80 °C up to 6 months, thus facilitating the adoption of 68Ga-THP-desIL2 into clinical practice. 68Ga-THP-desIL2 showed high affinity and specificity for CD25 on activated T-lymphocytes, particularly Tregs, thus opening new opportunities for imaging immune cells trafficking in the TME.

Class I KIT activating mutations are linked to mostly intracellular expression of aberrant MC immunophenotypes and the WDSM morphological pattern.

Our findings support the temporally optimized use of CD25-biased IL-2-based therapeutics in combination with ICIs for cancer immunotherapy.

Furthermore, this method improves T cell adherence, proliferation, and functional effectiveness, offering a potential foundation for advancing CAR-T cell therapies aimed at solid tumors. Future research should concentrate on optimizing culture conditions and testing this method in preclinical animal models to ensure its clinical applicability and efficacy.