CCL4 (Chemokine (C-C motif) ligand 4)

MSK AEs represent a common, under-recognized toxicity affecting nearly one-third of BCMA CAR-T recipients, often causing severe and prolonged disability. The identification of predictive baseline PMN-MDSC reduction and persistent inflammatory cytokine elevation provides insights into pathophysiology and suggests potential for risk stratification and targeted therapeutic intervention. These findings warrant prospective validation and development of standardized assessment and management protocols.

Comprehensive single-cell analysis identified selective chemokine recruitment signatures supporting γδ T-cell infiltration but revealed paradoxical corecruitment of immunosuppressive populations. Patient stratification through chemokine profiling, combined with γδ T-cell enrichment and targeted chemokine antagonism, represents a rational therapeutic strategy.

Host gene variants involved in trafficking (FYCO1 and RAB7A) and immune signaling (FOXA2, SFTPD, STAT3, and TET2) were associated with differential infection profiles. These findings show that SARS-CoV-2 induces variant- and tumor-specific morphological and immunological changes in cancer PDOs, highlighting the potential of this model to unravel host-virus interactions and identify genetic factors that shape infection outcomes in cancer.

Plasma proteomics revealed shared mediators including interleukin-6 and EN-RAGE across anatomical sites and ages. Together, our findings delineate anatomical-specific and age-specific immune programs in sepsis, highlighting candidate targets for precision immunotherapy.

These findings provide novel insights into the immunomodulatory effects of IORT and may have implications for optimizing multimodal treatment strategies for malignant brain tumors. As an exploratory study with a limited sample size, the findings should be interpreted as hypothesis-generating.

Our differential gene and signaling pathway analysis revealed the potential tumor-promoting mechanisms. These insights may offer new perspectives for clinical strategies targeting macrophages or the tumor microenvironment to treat brain metastasis of lung cancer.

In vitro, CXCL10 significantly improved BMMC migration in a dose-dependent manner, supporting clinical findings that elevated CXCL10 levels are associated with favorable healing in apical lesions. Although this study was limited by the small sample size and exploratory design, the cytokine profile of periapical lesions may be useful for assessing the condition of periapical lesions and modulating the immune response to bacterial infection.

Moreover, its combination with anti-PD1 therapy resulted in synergistic antitumor efficacy. This work represents the first report of a half-sandwich metal-based complex that targets the Wnt/β-catenin pathway to sensitize tumors to immune checkpoint blockade (ICB), offering a novel approach for designing metal-based chemoimmunotherapeutic agents.

Targeting this axis using an anti-Ly6G antibody to deplete neutrophils, a CRISPR/Cas9-mediated approach to conditionally knockout Ccl3/Ccl4 in neutrophils, and BX471 treatment to inhibit CCR1 in cancer cells all significantly reduced breast cancer lung metastasis. Together, this study not only demonstrates a stress-neutrophil-cancer axis that promotes lung metastasis in breast cancer but also provides potential strategies for reducing lung metastasis by targeting CSP neutrophils or CCR1+ breast cancer cells.

The formulation co-delivered NMS-873 (NM), a VCP/p97 inhibitor, to induce endoplasmic reticulum stress (ERS) and proteostasis collapse, together with bispecific PD-L1/CTLA-4 aptamers (P1C4) for dual checkpoint blockade. A complementary SLN formulation encapsulating galunisertib (G) and DNase (DN) degraded neutrophil extracellular traps (NETs) and suppressed tumor-associated neutrophils (TANs), thereby reshaping the immunosuppressive TME...In vivo PET/MRI imaging and immunohistopathological analyses confirmed selective tumor accumulation and effective tumor regression. This peptide-guided, TME-tailored SLN strategy achieves coordinated immune reprogramming, ERS induction, EMT/CSC reversal, NET disruption, and dual checkpoint blockade, offering a clinically translatable platform to overcome chemoimmunotherapy resistance in EGFR/PD-L1/CTLA-4-driven CRC.

The levels of several of the inflammatory mediators assessed in this study were elevated to a similar extent in both healthy males and females and those with acute MPS.

This study provides a comprehensive evaluation of a TCM-based multi-herb formulation for its immunomodulatory and antioxidant effects in lung cancer. HBK significantly enhanced anti-tumor immunity, increased antioxidant enzyme and cytokine activity, and remodeled the tumor microenvironment. Notably, these effects were mediated through inhibition of the TLR3/NF-κB signaling pathway. While individual herbal components have previously been linked to this pathway, our study is the first to demonstrate that a TCM-based multi-herb formula can modulate tumor immunity via TLR3/NF-κB inhibition in vivo.