CCL2 (Chemokine (C-C motif) ligand 2)

These findings suggest that placental sEVs play a critical role in modulating astrocyte responses to oxidative stress and mitochondrial dysfunction. The ability of sEVs to restore redox homeostasis highlights their potential physiological function in fetal neuroprotection against environmental stressors.

In summary, this study presents a novel stem cell delivery strategy that enables direct immobilization of MSCs at bone defect sites. Compared with non-electrospun MSCs, electrospun MSCs enhance autologous stem cell homing and modulate immunity to improve the osteogenic microenvironment, thereby promoting bone repair.

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.

Combined serum MCP-1 and hs-CRP levels could predict all-cause and cause-specific mortality rates in the general population.

Mechanistically, Tus inhibited tolimidone-induced Lyn kinase activation and suppressed SP-and Tween 80-induced β-hexosaminidase release, exhibiting an inhibitory profile comparable to that of the Lyn/Btk antagonist bosutinib. Additionally, Tus attenuated the phosphorylation levels of MRGPRX2 downstream signal molecules, including Btk, PLCγ1, PKC, p38 MAPK, IκB-α and NF-κB (p65). In conclusion, Tus attenuates SP-and Tween 80-induced mast cell activation and pseudo-allergic reactions by targeting the Lyn/Btk/PLCγ1 and p38/NF-κB pathways, highlighting its therapeutic potential for pseudo-allergy.

In summary, our results should encourage further clinical research to design corticosteroid regimens that optimize treatment of CAR T-cell toxicities while maintaining anti-malignancy activity.

We further detail past and ongoing therapeutic efforts and trials addressing these axes in both PDAC and relevant non-PDAC settings via several small-molecule antagonists and monoclonal antibodies: BMS-813160, Maraviroc, Leronlimab, FLX475, PF-07054894, IDOR- 1117-2520, and CAP-100. Despite continuous advances in the field, the current body of evidence remains limited and presents significant research gaps in areas such as spatial profiling, stage-specific analyses, and general mechanistic validation in PDAC-specific settings. Addressing these shortcomings will be key to developing a more comprehensive knowledge of the field and improving future therapeutic strategies to overcome PDAC.

The LPS group (5 mg/kg, intratracheal) was assigned to either prophylactic regimens (daily saline, dexamethasone 5 mg/kg, or digoxin 1 mg/kg, administered intraperitoneally for 5 days prior to LPS) or therapeutic regimens (same interventions initiated 12 h post-LPS for 3 days). At the study endpoint, pulmonary edema (wet-to-dry ratio) and lung injury pathways were analyzed in lung homogenates, including tumor necrosis factor-alpha (TNF-α), IL-6, myeloperoxidase (MPO), malondialdehyde (MDA), NF-κB (p65) DNA-binding activity, C-X-C motif chemokine ligand 2/macrophage inflammatory protein-2 (CXCL2/MIP-2), and hypoxia-inducible factor-1 alpha (HIF-1α), alongside histopathological evaluations. It also strongly inhibited NF-κB activation, reducing CXCL2/MIP-2, while decreasing HIF-1α in both regimens (each p < 0.001). Histological analysis corroborated these findings, revealing improved alveolar architecture and reduced inflammatory injury. In conclusion, digoxin exhibits potent immunomodulatory activity in experimental ALI, warranting further translational research focused on dose optimization and safety profiling.

In pregnant mice, maternal DHA supplementation mitigated LPS-induced FGR by suppressing NF-κB-mediated inflammatory signaling, modulating gut microbiota composition, and supporting intestinal barrier function, highlighting a potential nutritional strategy to alleviate inflammation-associated adverse pregnancy outcomes.

Our findings indicated that S100A14 is a clinically relevant biomarker for early detection and a potential therapeutic target for BrM.

MCP-1 enhances AKT phosphorylation and cell proliferation, suggesting a link between immune signalling and follicle activation. These findings indicate that LPS-induced activation of TLR4 may interact with PI3K-AKT signalling to regulate primordial follicle activation and ovarian reserve maintenance.

We also assess challenges in clinical translation, including tumor-type heterogeneity, insufficient biomarkers, and incomplete understanding of spatial immune architecture within bone lesions. Advancing myeloid-targeted interventions may enable more durable control of metastasis and improve outcomes for patients with skeletal involvement.