FCGR3A (Fc Fragment Of IgG Receptor IIIa)

P2, N=40, Withdrawn, Sydney Local Health District | Not yet recruiting --> Withdrawn

Furthermore, polarization of CAR-Ms into a proinflammatory state significantly enhanced tumor-killing efficacy, particularly in FCGR2A CAR-Ms. These findings highlight the potential of FCGR2A as an optimal signaling domain for CAR-M design and underscore the therapeutic promise of proinflammatory polarized CAR-Ms in solid tumor immunotherapy.

Furthermore, we demonstrate that VIF-Ig can accommodate VHHs to target various epitopes. Thus, this versatile modular platform is suitable for developing next-generation NK cell or even other cell engagers with enhanced efficacy and tunable specificity, especially for emerging multi-specific immune cell engagers.

This study establishes a foundation for understanding MRCRRG molecular mechanisms in OC. The identified subtypes, prognostic model, immune landscape alterations, and enriched pathways offer valuable insights for future experimental validation and potential diagnostic/therapeutic strategies.

Nevertheless, ADCC boosted the capacity of cDC1 and DC2 to prime naïve T cell responses but not of DC3. Thus, our data suggests that the therapy with bispecific antibodies targeting NK cells may have the potential to facilitate adaptive antitumor immune responses via activation of cDC1 and DC2.

A decrease in their number worsens pain intensity, possibly by altering the CD4⁺/CD8⁺ T cell balance. In contrast, NK cell reductions in T cell-deficient rats may contribute to hypersensitivity in the absence of T cells.

Proteomic analysis is helpful for discovering new protein markers. Using a combination of FHL3, CSRP2, and FCGR3A can increase the accuracy of the pathologic diagnosis of differentiated gastric adenocarcinoma with low-grade atypia.

This study provides the single-cell atlas of PBMCs in GP-NSV, uncovering profound transcriptional and compositional alterations across multiple immune cell subsets in active vitiligo. These findings offer novel insights into systemic immune dysregulation in GP-NSV and pave the way for novel targeted therapeutic strategies.

Overall, this study establishes a modular, nongenetically engineered uCAR-like NK platform that couples targeted recognition with enhanced tissue access. These findings highlight the potential of anti-MSLN CAR-like NK cells, particularly uCAR-like NK cells with enhanced tumor penetration, as promising therapeutic strategies for MSLN-positive solid tumors and lay the foundation for future clinical applications.

In xenograft MM tumor models in immunodeficient mice, NK cells derived from human peripheral blood and expanded in vitro were combined with BiKE and cGAS-STING signaling agonists, demonstrating effective anti-tumor activity and inhibition of MM cell proliferation. Collectively, the combination of cGAS-STING agonists and LILRB4-targeting NK cell engagers offers a promising approach for treating relapsed/refractory MM.

Proteomic analysis of VS patient plasma identified several disease-classifying biomarkers. Hepcidin warrants further investigation into its role in VS progression.

F9H4 combining with cetuximab also inhibits murine lung carcinoma growth in Fc gamma receptor-humanized mice, and such effect is mediated by NK cells and macrophages. The efficacy of F9H4+cetuximab in lung cancer models is the proof-of-concept for this new approach that promotes anti-tumor functions of Fc-enabled antibodies.