IL15 (Interleukin 15)

Allo-HCT can be a platform for treating NBL using combination ex vivo stimulated allogeneic NK cell therapy with TIM-3 blockade to enhance the GVT effect without inducing GVHD.

Furthermore, we show that intratumoral injection of IL-15 complexes traffics to the tumor-draining lymph node, as evidenced by Light sheet microscopy, and colocalizes with the anti-PD-1 monoclonal antibody. We also identify the immune signatures, localization, and distribution of immune cells in regressing and non-regressing breast tumors.

Imaging cytometry and single-cell transcriptomics revealed IFNγ-dependent macrophage reprogramming and IL-15 secretion, establishing a feed-forward loop that augments T cell functionality. A machine learning model trained on ex vivo cytotoxicity and transcriptomic data predicted patient responsiveness, supporting data-driven clinical stratification for solid tumour immunotherapy.

While the literature suggests these cytokines are not as beneficial or potentially harmful as single agents, when used in GI cancer treatment as an adjuvant in combination therapies or with innovative delivery methods, there is statistically significant therapeutic efficacy with improved clinical outcomes, median survival, and tumor suppression. The applicability of anti-tumorigenic cytokines (IL-12, IL-15, IL-2, and IFN-γ) as biomarkers of diagnosis and indicators of prognosis is being recognized with emphasis on their capabilities as therapeutic targets and adjuvant therapies in GI cancers.

KL130008 demonstrated potential for sustained efficacy and safety in the treatment of RA.

While muscle loss in newly diagnosed hyperthyroidism patients did not significant impair short-term explosive power, it may reduce endurance during sustained high-intensity exercise. The hyperthyroid state markedly altered exercise-induced immunometabolic dynamics, underscoring the need for comprehensive consideration of hyperthyroidism's complex physiological impact when designing personalized exercise regimens.

This process augments the antitumor immunity of NK cells while concurrently enhancing their antibacterial function, leading to intensified clearance of Fn and further alleviation of immunosuppression, thereby creating a positive feedback loop. The LYC@Bac biohybrid offers a precise strategy to modulate intratumoral microbiome-immune cell interactions, providing a promising approach for enhanced cancer immunotherapy.

In conclusion, metabolic engineering, leveraging its impact on epigenetic regulation during CAR T cell manufacturing, is crucial for generating potent, persistent, and functionally resilient products. This approach holds immense promise for expanding the curative potential of CAR T cell therapy to a broader range of cancers, particularly challenging solid tumors.

The lack of an intact immune system likely allows for unchecked in vivo expansion of cytokine armored CAR-NK cells, leading to early mortality in immunodeficient mice following treatment with these cells. We speculate that the use of humanized mice will allow for engraftment of tumor and alleviate cytokine armored CAR-NK toxicity, thereby allowing for effective assessment of CAR-NK efficacy in the absence of toxicity.

B1.23.2 treatment of the human KLM-1 pancreatic cancer model in humanized (NSG-IL15) mice provides evidence of suppression of tumor growth. Such anti-MHC-I mAb that block inhibitory KIR/HLA interactions may prove useful for tumor immunotherapy.

Consistently, expression of IL-15 resulted in blockade of tumor progression in the TKP CCA model. These findings highlight the importance of oncogenic Kras in CCA tumor maintenance and underscore KRAS inhibition as a potential therapeutic approach for CCA.

Our findings suggest that IL-15 levels could serve as a biomarker for identifying ESCC patients who are likely to benefit from RT and IM. These results also provide a rationale for targeting IL-15 as a novel therapeutic strategy to enhance treatment outcomes for ESCC patients.