IL7 (Interleukin 7)

Specifically, this senescence-like state is driven by PRELID1 and VDAC3 through their cooperative regulation of mitochondria-lysosome interactions in Bgc cells, which enhances IL-7 secretion and promotes functional crosstalk with CD8+ T cells to sustain antitumor immunity. In summary, our findings support a combinatorial strategy integrating targeting of the PRELID1-VDAC3-IL-7 axis in senescence-like Bgc cells with anti-PD-L1 immunotherapy for colorectal cancer.

These findings may suggest that early immune reconstitution of NK cells and γδ T cells is influenced by the bioavailability of IL-15 after HCT and that IL-15 could have a mechanistic effect in the activity of these innate effector cells. NK cells and γδ T cells are currently being investigated in several promising treatment settings, and IL-15 here may offer a potential benefit.

To overcome these challenges, here we develop a treatment strategy we term "expand and pull," which uses systemic administration of rhIL-7-hyFc, a long-acting recombinant human interleukin-7, to increase peripheral T cell abundance ("expand"), followed by intratumoral oncolytic virus treatment to recruit these cells to the tumor microenvironment ("pull")...We observe similar survival efficacy in experiments using a safer, genetically modified Δ10 3'-UTR ZIKV, as well as the clinically tested oncolytic adenovirus, Delta24-RGD. Collectively, our findings demonstrate that augmentation of both the systemic and local immune responses improves the utility of GBM-targeted immunotherapies.

In conclusion, this study proposes an innovative methodology that utilizes engineered sEVs for the co-delivery of protein antibodies and genetic materials. This approach establishes a promising strategy for advancing cancer immunotherapy by targeting the modulation of autophagy.

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.

FKBPL-based peptide mimetic, AD-01 (1 nM), in high-glucose conditions, upregulated endothelial vcam1 and glut1 mRNA expression, independent of miR-302b-5p. FKBPL plays an important role in glucose metabolism, endothelial function, angiogenesis, cardiac inflammation and function, and could be explored as a therapeutic target of cardiovascular disease both in nondiabetes and diabetes settings using precision medicine approach.

Treatment with ASP9801 alone or plus pembrolizumab was generally well tolerated; however, the study was stopped due to lack of efficacy during dose expansion.

This meta-analysis demonstrates that myokine responses following endurance exercise are clearly increased and moderated by factors such as exercise duration, intensity, exercise type, and training status, allowing their targeted modulation for therapeutic use. Even "suboptimal exercise conditions" can elicit significant increases in immunoregulatory myokines, thereby promoting beneficial immune responses, suggesting that endurance exercise is a key component in the treatment of a wide range of diseases.

Notably, 7 × 19 CAR-T cells derived from allogeneic donors also induced epitope spreading in tumor-bearing hosts, thereby increasing survival. The 7 × 19 CAR system is a promising strategy for overcoming antigen heterogeneity in solid tumors by promoting epitope spreading.

In contrast, ibrutinib added 48 h post-activation did not show these effects. These findings suggest that caution should be exercised when incorporating ibrutinib into ex vivo expansion system for adoptive non-genetically engineered T cells or combining ibrutinib with these T cell immunotherapies in clinical trial settings.

In conclusion, IL-7 induces EMT to promote growth and metastasis NSCLC via the activation of Notch1/TGF-β pathway. IL-7 may be a potential target against human NSCLC.

Consistent with prior preclinical studies, we demonstrate that dasatinib and ponatinib, unlike SRC sparing TKIs (imatinib, nilotinib), antagonize blinatumomab's T-cell engaging efficacy by potently inhibiting LCK Y394 phosphorylation, a critical step in proximal TCR signaling. We show that TKI-induced T-cell suppression and antagonism can be significantly improved by supplementing co-cultures with common gamma-chain cytokines, particularly IL-7. IL-7 robustly enhances human T-cell proliferation, reduces exhaustion, and significantly improves blinatumomab's cytotoxic efficacy in the presence of Src/BCRABL1 TKIs.