Tumor necrosis factor α (TNFα) is a highly pleiotropic cytokine with a variety of biological functions such as cell proliferation, metabolic activation, inflammatory response and cell death. TNFα can induce a variety of mechanisms to initiate hepatocyte apoptosis, resulting in subsequent liver damage. HBsAg is the most abundant HBV protein in the hepatocyte during chronic virus infection. However, its role in TNFα-mediated apoptosis of hepatocytes has not been revealed. We report here that HB...

CD8⁺ T cell exhaustion during chronic infection and cancer is marked by impaired effector function and limited responsiveness to stimulation. While memory CD8⁺ T cells can be activated TCR-independent...

Li et al. show that the SARS-CoV-2 SUD2core domain binds the neutrophil protein HEBP2 and recruits the E3 ligase LTN1 to trigger its degradation, thereby activating the Rab27a-SYTL1 axis to drive pathogenic neutrophil degranulation, NETosis, and cytokine release. Small-molecule inhibitors of this interaction attenuate neutrophil-mediated inflammation.

Researchers identify the cytokine-mediated mechanism sustaining CD8+ T cell inflammation in lupus kidneys, opening pathways for targeted immunotherapy.

Membranous nephropathy (MN) is a rare autoimmune kidney disease mediated by autoantibodies directed against podocyte antigens, such as phospholipase A2 receptor type 1 (PLA2R1). MN exhibits marked cli...

Type 2 cytokines suppress antitumor immunity through coordinated effects on T cells and dendritic cells. Fabre et al. show that combined blockade of IL-4, IL-13, and TSLP enhances PD-1 checkpoint inhi...

Type 2 cytokines suppress antitumor immunity through coordinated effects on T cells and dendritic cells. Fabre et al. show that combined blockade of IL-4, IL-13, and TSLP enhances PD-1 checkpoint inhibition, promotes immune remodeling in tumors, and is supported by human data linking type 2 signaling to poor cancer outcomes.

Aims: Δ133p53α is a naturally occurring isoform of the human p53 protein that inhibits p53-mediated cellular senescence. We previously reported that transgenic expression of this senescence-inhibitory p53 isoform counteracts aging-associated pathological changes in progeria model mice (heterozygous LmnaG609G/+). The anti-aging effect of Δ133p53α was attributed in part to reduced levels of the proinflammatory cytokine IL-6. This study aims to comprehensively profile Δ133p53α-induced changes in cytokines and chemokines.Methods: A Luminex-based multiplex quantitative assay was performed using mouse serum samples from transgenic Δ133p53α-expressing LmnaG609G/+ mice and non-expressing controls. Quantitative RT-PCR and RNA in situ hybridization assays were used to assess Cxcl10 expression in mouse tissues. In addition, gene expression datasets from human tissues were analyzed.Results: In the Luminex assay, used as an exploratory screen, transgenic Δ133p53α expression was suggestively associa

A study of hundreds of thousands of UK adults traces connections between inherited susceptibility, smoking, body fat, mental health, socioeconomic conditions, inflammatory proteins, and subtle changes in heart structure and function. Study: Gene–environment interactions shape cytokine-mediated inflammation and cardiovascular risk Genetic susceptibility may modify the association between environmental exposures and systemic inflammation and cardiovascular risk, according to a new study published in the European Journal of Preventive Cardiology. Background Chronic low-grade inflammation is a major hallmark of cardiovascular disease. Chronic inflammation has been associated with harmful changes in the heart structure and function, which are linked to an increased risk of heart attack and stroke even in individuals without clinically diagnosed cardiovascular disease. Genetic and environmental risk factors are strongly associated with chronic systemic inflammation. Yet, it remains largely unknown how specific environmental risk factors interact with genetic risk factors to shape the association between chronic inflammation and cardiovascular outcomes. Researchers at Imperial College London, UK, analyzed blood biomarkers, genetic profiles, cardiac imaging data, environmental exposure variables, and cardiovascular outcomes across subsets of up to 488,079 UK Biobank participants to identify specific inflammatory mediators that are associated with adverse cardiovascular events and to explore how environmental and genetic risk factors...

AbstractBackground. Chronic inflammation is a major driver of cardiovascular diseases, but mechanisms linking systemic inflammation to cardiac remodelling

The dynamic interplay between pro- and anti-inflammatory cytokines plays a crucial role in regulating host immune responses. In our earlier study, we showed that Leishmania donovani-induced IL-33 destabilizes host cytokine dynamics by downregulating TNF-α and IL-12 and ensures intramacrophage parasite survival. Another pertinent host favorable proinflammatory cytokine is Il-1β, maturation of which depends on the activation of NLRP3 inflammasome complex. Our present study highlights that...

Acute rheumatic fever is an immune-mediated sequela of Streptococcus pyogenes (group A Streptococcus) infection, presenting with fever, arthritis, chorea, rash, and, crucially, carditis. Without effec...