CD86 (CD86 Molecule)

Our study identifies fibroblast-immune cell interactions, particularly IL-6-mediated fibroblast-macrophage crosstalk, as a key mechanism in radioimmunotherapy-induced cardiac fibrosis. Tocilizumab, an IL-6R inhibitor, demonstrates therapeutic potential to attenuate this cardiotoxicity.

These results suggest that E-BVL may influence apoptotic and proliferative pathways in THP-1 leukemia cells. Overall, this study highlights B. vulgaris leaf extract as a promising natural source of bioactive compounds for anti-leukemic research, without specifically implicating berberine, which was not detected in the extract.

These data demonstrate that a combination of CD47 blockade and anti-PD1 therapy enhances tumor antigen presentation and immune cell infiltration, while further improving anti-tumor responses in combination with tumor-targeted radiotherapy. This study provides support for the rational design of combinatorial immunoradiotherapy, using anti-CD47 inhibitors and anti-PD1 therapy, in a clinical trial targeting locally advanced HPV-negative HNSCC.

It was also linked to reduced cisplatin/paclitaxel sensitivity (P < 0.05) and lower immunotherapy response (29.04% vs. 45.05%, P = 0.015). These findings suggest that JAML deficiency may suppress cyclic GMP-AMP synthase (cGAS)-STING pathway activation, potentially contributing to M1/M2 macrophage polarization imbalance and facilitating EC progression. Clinically, JAML expression shows promise as a potential biomarker for prognostic stratification and treatment response prediction (chemotherapy/immunotherapy), providing insights for developing precision immunochemotherapy strategies in EC.

Although benzodiazepines, including midazolam, possess anti-inflammatory properties and suppress macrophage activity, the impact of Re on macrophage-mediated immune responses remains uncertain. Conversely, Re did not affect the phagocytic capacity of TGC-macrophages, as evaluated by fluorescein isothiocyanate-labeled dextran, even at concentrations that inhibited inflammatory cytokine production and costimulatory molecule expression in LPS-activated TGC-macrophages. These findings suggest that Re exerts anti-inflammatory effects without suppressing essential innate immune functions, such as phagocytosis by macrophages.

Our study demonstrates that a CLDN18.2-targeting DC vaccine can effectively induce potent antigen-specific CTL responses and elicit significant antitumor immunity in a preclinical model. These findings provide a strong rationale for the clinical development of CLDN18.2-directed DC-based immunotherapy for gastric cancer.

Functional analysis revealed that the pathways enriched in glioma tissues with high SLAMF9 expression were associated with immune response-related pathways. This study is the first to highlight the important clinical value of SLAMF9 in patients with glioma.

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.

7a induced apoptosis while upregulating the differentiation marker CD86 and downregulating the stem cell-associated proteins SOX2 and CD44. Collectively, these findings establish compound 7a, a tranylcypromine-pyrimidine derivative, provides the structural foundation for the development of LSD1 inhibitors for the treatment of AML.

In vivo, AQP4-IgG-induced EVs-mtDNA exacerbated microglial activation and NMO through the TLR9/MyD88/NF-κB pathway. AQP4-IgG-induced EVs carried mtDNA to upregulate TLR9, further activating the MyD88/NF-κB pathway, thereby promoting microglial activation and transition toward pro-inflammatory gene-high-expressing cells to drive NMO progression.

In addition, suppressing or overexpressing METTL3, YTHDF1, and NMDAR2B correspondingly decreased or increased these effects, but modulation of NMDAR2B did not change the expression of METTL3/YTHDF1. rTMS can affect the polarization state of microglia and neuroinflammation by regulating the METTL3/NMDAR2B/NLRP3 signaling pathway, thereby improving NeuP.

These results demonstrate that an RT-based combination therapy that robustly induces CD4+ T cells alongside CD8+ T cells can elicit a strong abscopal response and suggest that CD4+ effector T cells act at abscopal sites by promoting DC-mediated cross-presentation of tumor antigens to CD8+ T cells originating from the irradiated tumor.