IL-11 acts as a vaccine adjuvant in Nile tilapia (Oreochromis niloticus) against Streptococcus agalactiae, enhancing both cellular and humoral immune responses.

Background: Osteoarthritis (OA) is a prevalent and debilitating chronic disease for which there are currently no approved disease-modifying osteoarthritis drugs (DMOADs). While mesenchymal stem cells (MSCs) have emerged as promising DMOAD candidates, their clinical application is hindered by inconsistent in vivo efficacy and an incomplete understanding of the underlying pathological mechanisms and therapeutic targets. Methods: To address these limitations, we developed a novel therapeutic strategy by conjugating MSCs with steroid-loaded gold nanostars (MSC-Au-Steroid). The effects of MSC-Au-Steroid were assessed in vitro using osteoarthritis patient-derived chondrocytes and peripheral blood mononuclear cells (PBMCs), and in vivo using a monosodium iodoacetate (MIA)-induced mouse model of osteoarthritis. Key assessments included anti-inflammatory activity, metabolic profiling (glycolysis and oxidative phosphorylation), mitochondrial function, reactive oxygen species (ROS) production, mTOR signaling, and immunomodulatory effects on Th1, Th17, and regulatory T cells (Tregs). Results: MSC-Au-Steroid demonstrated strong anti-inflammatory effects in OA chondrocytes, promoted cartilage regeneration, and normalized altered metabolic profiles under inflammatory conditions. It improved mitochondrial function and suppressed excessive ROS production via mTOR signaling regulation. In vivo, MSC-Au-Steroid alleviated clinical symptoms and preserved cartilage integrity in the MIA-induced OA mouse model. Furthermore, it exhibited immunomodulatory effects in both mouse and patient-derived PBMCs, inhibiting Th1 and Th17 responses while promoting Treg induction and restoring immune tolerance. Conclusions: MSC-Au-Steroid represents a promising multifactorial therapeutic candidate for OA by targeting both metabolic reprogramming and immune modulation. These findings provide strong evidence that MSC-Au-Steroid acts as a disease-modifying agent, addressing multiple pathological factors and offering superior efficacy compared to current therapies.

Emerging roles of heme oxygenase 2 (HO-2) in cancer: Implications for diagnosis and therapy.

Multifunctional biliverdin-based MnO₂ nanozyme alleviates oxidative stress and immune rejection in islet graft protection.

Integrated m6A reader network in acute myeloid leukemia: prognostic modeling, immune modulation, and functional validation of YTHDF3.

Astaxanthin mitigates dibutyl phthalate-induced thyroid hormone disruption in zebrafish larvae via multi-target regulation.

Ferroptosis triggered by gill dysbiosis mediates immune failure in grass carp overwintering syndrome.

PapMV nanoparticles: A novel pathway to SARS-CoV-2 protection, distinct from Imidazoquinolines.

Gold-embedded yolk-shell mesoporous organosilica nanocomposite for microwave-enhanced targeted chemotherapy and immune modulation in hepatocellular carcinoma.

Sleep and fatigue complaints during pregnancy versus perinatal depression: Impact on toddler cognition.

Systemic Review of Inflammatory Pathways and Immune Modulation in Atherosclerotic Cardiovascular Disease.

Decoding preterm birth: Non-Invasive biomarkers and personalized multi-omics strategies.

Biophysical characterization of Hpa1 protein from Xanthomonas orzyae.

zDHHC-mediated palmitoylation modification patterns and tumor immune microenvironment infiltration characterization in pancreatic cancer.

Cardio-oncology has rapidly evolved in the past decade. It is a continuous field that was founded on the manifestation of cardiac dysfunction in patients treated with anticancer therapy. Short- and long-term cardiovascular complications became known as cancer therapy-related cardiovascular toxicity (CTR-CVT). These may arise from a plethora of anticancer therapies, including broad classes such as chemotherapy, immunotherapy, and hormonal therapy. Recently, the first European Society of Cardiology guideline on cardio-oncology was published, providing expert consensus on definitions, diagnosis, treatment, and prevention for health-care professionals. This side of cardio-oncology focuses on the classical CTR-CVT, here termed forward cardio-oncology. On the other side is the paradigm of heart failure stimulating tumor growth, coined as reverse cardio-oncology. As cardio-oncology expanded, the knowledge of co-occurrence of these disease entities in the same individuals grew. This raised the question of whether this phenomenon was due to shared risk factors (i.e. diabetes mellitus, obesity, etc.) between cardiovascular disease (CVD) and cancer or because of shared underlying mechanisms, and thus whether the presence of one of the two disease entities could drive the onset or progression of the other. Indeed, mechanistic studies revealed that heart failure can stimulate tumor growth in a multifaceted manner, including through a protumor cardiac secretome, by immune system modulation, or even through the gut microbiome. This review provides an extensive and robust overview of the current knowledge on the entirety of cardio-oncology and highlights future perspectives for research.

Background: Biglycan (BGN), a component of the extracellular matrix, has been closely associated with tumor progression. This study aimed to investigate the endocrine and paracrine roles of BGN in papillary thyroid carcinoma (PTC) to elucidate the underlying molecular mechanisms driving PTC development. Methods: Multi-omics integration was used to assess BGN expression and its clinical relevance in PTC. Functional assays, including cell viability, colony formation, and cell cycle analysis, were used to evaluate the biological functions of BGN. RNA-seq identified key signaling pathways involved in BGN-mediated PTC progression. Immune cell infiltration and macrophage polarization were analyzed using single-cell RNA-seq and flow cytometry. CRISPR interference was employed to suppress BGN enhancer activity, while luciferase assays confirmed NR2F2's role in regulating BGN expression. The therapeutic potential of the NR2F2-specific inhibitor CIA1 was tested in PTC cell lines and mouse models. Results: BGN overexpression in malignant PTC cells evaluated by BayesPrism deconvolution was linked to poor clinicopathological features in PTC. BGN knockdown inhibited cell proliferation and induced cell cycle arrest, which was rescued by recombinant BGN. Tumor-derived BGN activated the AKT signaling pathway, promoting tumor growth. Additionally, high BGN expression facilitated M2 macrophage polarization and immune evasion through TLR4 signaling. The NR2F2-BGN axis activated BGN transcription and AKT signaling. CIA1 treatment reduced BGN expression, suppressed cell proliferation, and modulated macrophage polarization. Conclusion: Our findings highlight the NR2F2-BGN axis as a critical regulator of PTC progression. Targeting this axis offers a promising therapeutic strategy for PTC treatment and immune microenvironment modulation.

This study employed an integrated untargeted metabolomics approach to identify resistanceassociated biomarkers in dwarf cashew (Anacardium occidentale L.) genotypes under black mold stress-a severe foliar disease caused by Pilgeriella anacardii Arx & Müller. Metabolomic profiling was performed using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MSE) and nuclear magnetic resonance (NMR) spectroscopy. This methodology enabled a comprehensive analysis of four dwarf cashew genotypes with varying resistance to P. anacardii: ‘CCP 76’ and ‘BRS 189’ were susceptible, ‘BRS 226’ was intermediate, and ‘BRS 265’ was resistant. Orthogonal partial least squares discriminant analysis (OPLS-DA) revealed clear metabolic segregation between resistant, susceptible, and intermediate genotypes, with high predictive power (R2 Y ≥ 0.98; Q2 ≥ 0.95). Resistant clones (BRS 265 and BRS 226) showed pronounced metabolic reprogramming, marked by increased accumulation of flavonoid glycosides (quercetin-3-D-glucoside, isoquercetin), flavan-3-ols ((+)-catechin, gallocatechin), galloylated glucose derivatives (penta- and tetra-O-galloyl-glucosides), and biflavonoids (amentoflavone, agathisflavone). These compounds function as antioxidants, membrane disruptors, metal chelators, enzyme inhibitors, and immune response modulators. Pathway enrichment analysis highlighted the activation of flavonoid and flavonol biosynthesis as central to resistance. Elevated sucrose levels in resistant genotypes suggest a role in energy supply and systemic signaling. Altogether, this metabolomic fingerprint supports a complex biochemical defense strategy and offers robust biomarkers for marker-assisted selection.

In multiple sclerosis (MS), a variety of immunosuppressive treatments are available. While effective, these approaches often lead to sustained impairment of essential components of the immune system, posing long-term safety concerns. Consequently, there is a growing interest in alternative therapeutic approaches that selectively limit pathogenic B-cell functions while preserving their physiologic roles. In this study, we investigated the therapeutic potential of inhibiting the enzyme Bruton tyrosine kinase (BTK), a key signaling molecule in both B-cell and myeloid cell activation. The effects of the BTK inhibitor evobrutinib were evaluated in various experimental in vivo models of CNS demyelination, each representing different aspects of disease pathology as well as a naïve healthy condition. The impact on disease onset and severity was determined, and phenotypical alterations in different cell populations were assessed via flow cytometry. Furthermore, functional changes in both murine and human myeloid cells induced by BTK inhibition under specific Fc receptor-dependent stimulation were analyzed in in vitro settings using flow cytometry. In a naïve, healthy environment, evobrutinib promoted the development of regulatory B-cell properties. In various experimental models of CNS demyelination, BTK inhibition limited the differentiation of proinflammatory B cells while supporting their regulatory properties. Beyond modulating B-cell responses, BTK inhibition also attenuated the activation of myeloid cells after Fc receptor-mediated antigen uptake, a process assumed to be of importance in conditions, such as neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein-antibody associated disease. In addition, BTK inhibition was shown to suppress the secretion of proinflammatory cytokines and reduce antigen presentation, further dampening pathogenic immune responses. These findings highlight the potential of BTK inhibition as a selective and sustainable immunomodulatory strategy for both B cells and myeloid cells in the context of chronic CNS inflammation. Despite their efficacy, broad-spectrum immunosuppressive therapies often fail to provide targeted immune modulation. By contrast, BTK inhibition promotes regulatory B-cell properties while leaving other B-cell functions intact, providing the basis for its broad use-potentially in combination with established anti-inflammatory agents.

Animal toxins and NETosis: A new frontier in innate immune modulation.

Single-cell RNA sequencing reveals beneficial mechanisms of Exendin-4 in autoimmune uveitis.