Our findings indicate that antigen-specific therapy with PS liposomes mimicking apoptotic bodies downregulates the MOG-specific inflammatory immune response and expands Breg and Treg cells, offering a safe, versatile, and easily applicable approach that strongly supports its potential for near-future clinical translation in MS.

This study demonstrates that adjuvants can facilitate recruitment of cDC1s to the peritoneal cavity, a feature that may contribute to the effectiveness of i.p. administration on elicitation of CD8 T cell responses. Furthermore, we demonstrate that CAF09b-induced CD8 T cell responses require BATF3-dependent cDC1 cells. Understanding cDC1 and CD8 T cell dynamics via different immunization routes may aid in the design of more effective vaccine strategies.

Mice with EC-specifically MYPT1-deficient (Mypt1ΔEC) also showed coronary endothelial hyperpermeability, and treatment with the S1PR1 agonist FTY720 failed in alleviating the pathological effects. At 1 month post-transverse aortic constriction, both Mypt1ΔEC and S1pr1ΔEC mice displayed aggravated pathological cardiac remodeling. These findings suggest that the S1PR1-MYPT1 signaling is crucial for coronary endothelial permeability and myocardial microenvironmental homeostasis under pressure overload, targeting which may offer therapeutic potential for related heart diseases.

Our research indicates that FTY720 may inhibit NSCLC via possible targets ZEB2 and S1PR1, further laying the theoretical foundation for the utilization of FTY720 in NSCLC treatment.

In vitro and in vivo experiments validated two repositioned drugs, Fingolimod and Piperlongumine, both targeting ECM components, significantly inhibited LSCC cell growth, proliferation and migration at concentrations below 10 μM. These results provide compelling evidence for the power of systems biology to identify subtype-specific therapeutic vulnerabilities. Our findings highlight a promising framework for precision oncology and underscore the potential of ECM-targeted interventions in LSCC.

P4, N=30, Recruiting, Novartis Pharmaceuticals | Trial completion date: Jan 2026 --> Sep 2027 | Trial primary completion date: Jan 2026 --> Sep 2027

The findings supported the applicability of brain organoids as a model system for drug screening studies for neuroinflammatory brain diseases.

P2, N=427, Completed, Viatris Innovation GmbH | Phase classification: P2b --> P2

P3, N=300, Not yet recruiting, Viatris Innovation GmbH

The results demonstrated that F4 inhibited the growth of CRC by maturing DCs through activating S1PR1-mediated phosphoinositide 3-kinase/protein kinase B and NF-κB pathways, which triggered the antitumor effects of CD8+ T cells. Therefore, F4 could serve as an antitumor immunomodulator for CRC treatment.

P=N/A, N=606, Completed, Novartis Pharmaceuticals

Microglia exert time- and region-specific effects on WMI after ischemic stroke. A nuanced understanding of their dynamic phenotypes and interactions with other glial elements is essential for developing targeted therapies. Future research should integrate single-cell technologies, human validation, and sex-specific analyses to refine microglia-based interventions.