Keep Current with the Latest in Cell Biology Research

MEK-Dependent Bioenergetic Demand Drives Terminal CD8+ T Cell Exhaustion

[Immunity] Investigators examined the pathways whereby chronic antigen stimulation leads to metabolic dysfunction. Chronic T cell receptor (TCR) engagement increased ATP demand, leading to mitochondrial NADH accumulation, accumulation of reactive oxygen species, and subsequent mitochondrial dysfunction.

PD-1 Blockade Unleashes Local Hepatitis B Virus-Related B Cell Response Inhibiting Hepatocellular Carcinoma

[Cancer Cell] Researchers conducted a mechanistic study parallel to their Phase II trial of perioperative anti-PD-1 therapy in patients with resectable recurrent hepatocellular carcinoma to study its mechanism of action.

Neutrophil Extracellular Traps Induced by Tumor-Derived NGAL Reprogram CAF Subtypes via ITGA5 to Promote Tumor Progression in Pancreatic Cancer

[Gut] Scientists delineated how neutrophil extracellular traps (NETs) instruct cancer-associated fibroblast subtype specification and immunosuppression in pancreatic ductal adenocarcinoma, identify upstream NETosis drivers and evaluate combinatorial therapeutic strategies targeting this axis.

Nrf2-Mediated Metabolic Reprogramming Drives Regulatory T Cell Accumulation in Hepatocellular Carcinoma

[Nature Communications] The authors investigated how the development of hepatocellular carcinoma impacts the molecular programmes of tissue-resident Tregs.

Regulation of Neutrophil Homeostasis by the TNFAIP8 Family of Polarity Proteins

[Cell Reports] Researchers reported that TNF-α-induced protein 8 (TNFAIP8) family of polarity proteins regulates neutrophil homeostasis by propagating phosphoinositide signaling.

Disrupting Treg Lineage Stability Elicits RORgT-Mediated Plasticity and Enhances Anti-Tumor Immunity

[Cell Death & Disease] Scientists designed, validated, and employed a novel genetically modified mouse model to conditionally ablate the Hedgehog gene, Gli2, specifically in Tregs.

CAR19 Tregs Treat Murine Chronic Graft-Versus-Host Disease through Immune Suppression in Absence of Measurable B-Cell Cytolysis

[JCI Insight] The authors evaluated human CD19-directed chimeric antigen receptor (CAR19) T cell therapy in a clinically relevant murine chronic Graft-Versus-Host disease model with bronchiolitis obliterans syndrome.

STIM1-Dependent Treg Dysfunction Promotes Cardiometabolic HFpEF: Insights from Patients and Animal Studies

[Cardiovascular Diabetology] Researchers identified Treg stromal interaction molecule 1 (STIM1) as a key driver of immune-mediated heart failure with preserved ejection fraction (HFpEF) progression and provided mechanistic evidence from humans to mice supporting immune-targeted therapeutic strategies.

KLF5-Driven TAZ-FASN Signaling Reprograms Fatty Acid Metabolism to Support Treg Differentiation in Lung Cancer

[Journal of Translational Medicine] Scientists revealed a KLF5-driven fatty acid metabolic program in lung cancer. Krüppel-like factor 5 (KLF5) cooperates with TAZ to activate FASN transcription, thereby increasing lipogenesis and free fatty acid release.

Selective Depletion of Tumor-Infiltrating CD4+CCR8+ Tregs by AZ084, a Novel CCR8 Antagonist

[Cancer Science] Investigators demonstrated that CCR8 is preferentially expressed on tumor-infiltrating CD4+ Tregs in syngeneic ID8 and B16 tumor models, accounting for a significantly higher proportion compared with CD4+ conventional T cells and CD8+ T cells (p < 0.001).

The Future of TCR-Treg Therapies Is Renewables

[Autoimmunity Reviews] The authors highlight emerging solutions for closed, automated, and decentralised production and discuss allogeneic approaches using gene-edited or banked Tregs with HLA engineering or matching.

Macrophage Autophagy in Allergic Diseases: Regulatory Mechanisms, Immune Crosstalk, and Therapeutic Implications

[International Immunopharmacology] Scientists systematically synthesize the molecular mechanisms governing macrophage autophagy and its dual role in allergic diseases, including allergic rhinitis, asthma, and atopic dermatitis.

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