- Context-dependent lysophosphatidic acid signalling in inflammation: evidence hierarchy, myeloid regulation and translational gaps. [Review]
- CONCLUSIONS: LPA should not be classified as simply pro-inflammatory or anti-inflammatory. Anti-inflammatory LPA models should be regarded as experimentally plausible but translationally unproven until validated using defined LPA species, receptor-resolved perturbation and concentration-resolved human myeloid-cell systems.
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- MICA gene modulates immune microenvironment and comorbid mechanisms in diffuse large B-cell lymphoma and primary Sjögren's syndrome. [Journal Article]
- CONCLUSIONS: MICA plays a key role in shaping the immune microenvironment of DLBCL and PSS. By reinforcing anti-tumor immune responses and limiting tumor growth, it emerges as a promising biomarker and therapeutic target in both diseases.
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- NKR[+]CD8[+] T cells and iNKT cells protect mice from AOM/DSS-induced colorectal cancer under conditions of IFNγ-mediated hyperinflammation. [Journal Article]
- CONCLUSIONS: NKR[+]CD8[+] T cells in Yeti mice with elevated IFNγ levels suppress CRC development in an iNKT cell-dependent manner, suggesting that NKR[+]CD8[+] T cells and iNKT cells cooperate to drive optimal anti-tumor immune responses against CRC during IFNγ hyperinflammation. Our findings highlight a potential immunotherapeutic strategy for CRC by reinforcing IFNγ-dependent anti-tumor responses.
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- TRPV4/IP3R-1-mediated endothelial pyroptosis drives pulmonary microvascular endothelial permeability in endotoxin-induced acute lung injury. [Journal Article]
- CONCLUSIONS: TRPV4 disrupts HPMEC integrity via IP3R-1 and triggers GSDMD-mediated pyroptosis through a Ca[2+]-dependent mechanism, exacerbating LPS-induced ALI.
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- Effect of gut bacterial extracellular vesicles on angiogenic potential and vascular integrity: positive and negative aspects. [Review]
- Extracellular vesicles (EVs) are intercellular mediators in prokaryotic and eukaryotic systems that have the potential to regulate various physiological and pathological processes in recipient cells. Among them, bacterial extracellular vesicles (BEVs), including Gram-negative outer membrane vesicles (OMVs) and Gram-positive membrane vesicles (MVs) produced by the gut microbiota, have special role…
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- International comparison of neutrophil surface markers after severe trauma is feasible using point of care flowcytometry - results from a pilot study. [Multicenter Study]
- CONCLUSIONS: This study demonstrates the successful implementation of a fully automated PoC neutrophil analysis infrastructure from one trauma center to another facilitating multicenter flow cytometry studies. This paves the way for advanced immune monitoring that could significantly improve personalized clinical decision-making.
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- Regulation of Tph cell differentiation via farnesoid X receptor of dendritic cells in inflammatory bowel disease. [Journal Article]
- CONCLUSIONS: Tph cell levels were elevated in inflamed intestinal tissues. FXR suppression in BMDCs was associated with activated PPAR-γ signaling; and with reduced DC maturation, IL-12 secretion, and Tph cell differentiation.
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- SERPINE1 in ARDS: an emerging regulator of inflammation-coagulation-fibrinolysis crosstalk. [Review]
- CONCLUSIONS: SERPINE1 is a potentially important integrative regulator and biomarker of dysregulated inflammation, coagulation, and fibrinolysis in ARDS. Future studies should clarify its causal, cell-specific, and phenotype-dependent roles to facilitate the development of targeted therapeutic strategies.
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- Autosomal recessive A20 zinc finger 7 mutation is associated with early-onset lupus-like disease. [Journal Article]
- CONCLUSIONS: Our findings characterize a critical mutation associated with early-onset lupus-like disease in its recessive form and continue to highlight the important role of A20 in maintaining immune homeostasis.
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- Niflumic acid suppresses NLRP3 inflammasome activation by limiting chloride efflux and mitochondrial ROS production. [Journal Article]
- CONCLUSIONS: NFA suppresses NLRP3 inflammasome activation through a mechanism associated, at least in part, with TMEM16F-related chloride efflux and mtROS production. These findings suggest an anti-inflammatory mechanism of NFA that is not fully explained by canonical COX inhibition and support further investigation of NFA as a potential modulator of inflammasome-associated inflammation.
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- Lipopolysaccharide-mediated macrophage polarization, conserved pathogenesis, and implications for peripheral neuropathy: a systematic review. [Systematic Review]
- CONCLUSIONS: These findings demonstrate conservation of LPS-driven M1-like macrophage polarization and tissue injury across systems, supporting the need to further investigate the biological plausibility of a gut-immune-nerve axis contributing to peripheral neuropathy.
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- Myeloid PKM2 deficiency alleviates allergic airway inflammation and promotes macrophage efferocytosis via SLC13A3. [Journal Article]
- CONCLUSIONS: Our study reveals a novel role for myeloid cell-specific PKM2 and SLC13A3 in asthma, linking efferocytosis to immune metabolism during allergic inflammation.
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- IGF2BP1 modulates ZDHHC5-mediated NLRP3 inflammasome activation to promote mitochondrial damage and foam cell formation of vascular smooth muscle cells. [Journal Article]
- CONCLUSIONS: IGF2BP1 regulates ZDHHC5-mediated NLRP3 inflammasome activation, thereby enhancing mitochondrial damage and foam cell formation in vascular smooth muscle cells, which provides new therapeutic targets for AS.
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- From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases. [Review]
- CONCLUSIONS: Current research on cuproptosis in AIDs is largely correlative, bioinformatic, or model dependent, and is insufficient to confirm canonical cuproptosis as a primary pathogenic mechanism in AIDs. Cuproptosis should be regarded as a conditional and hypothesis-generating framework. Future studies should adopt a rigorous evidence hierarchy, optimize diseaserelevant model selection, and validate its pathophysiological significance through direct biochemical assays. The clinical translation of copper-targeted therapeutic strategies still requires substantial foundational and clinical research support.
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- Integrative multi-omics identifies CYP1B1 as a candidate molecular link between toxicant exposure and ferroptosis-related epithelial stress in COPD. [Journal Article]
- CONCLUSIONS: Integrative multi-omics and experimental analyses identified CYP1B1 as a candidate COPD-associated epithelial stress biomarker linked to ferroptosis-related signatures in airway secretory cell populations. The findings suggest a potential association between cigarette-smoke-induced CYP1B1 upregulation, lipid peroxidation-related epithelial injury, and epithelial remodeling in COPD. However, CYP1B1 should be considered an exploratory biomarker and putative mechanistic node rather than a validated diagnostic tool or therapeutic target at this stage. Further studies using larger clinically annotated cohorts, smoking-adjusted analyses, cell-type-specific perturbation, ferroptosis rescue experiments, and pharmacological validation are needed.
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