Ruling supports Brussels regulators findings over dominance of tech giant’s Android mobile operating system

Extracellular vesicles (EVs) play a role in intercellular communication, however the precise biogenesis of different populations of EVs are not clear. Here, the authors follow the intracellular t...

Arf GTPase-Activating proteins (ArfGAPs) mediate the hydrolysis of GTP bound to ADP-ribosylation fac

Background and aims Oncogenic KRAS mutations are present in approximately 90% of pancreatic ductal adenocarcinoma (PDAC). However, Kras mutation alone is insufficient to transform precancerous cells i...

Read the full paper: MGAT5 drives melanoma aggressiveness via TIMP1 glycosylation–dependent CD63–β1-integrin signaling

Severe Omicron cases present profound lymphocytopenia, suggesting variant-specific immune injury. We identify CD63 as a conserved T-cell host factor supporting ACE2-independent SARS-CoV-2 entry. Despite lower intracellular viral loads than the ancestral strain, Omicron elicits enhanced T-cell apoptosis largely through a bystander mechanism. Omicron-stimulated epithelial cells secrete GDF15, which upregulates the pro-apoptotic protein BCL2L13 in T cells and thereby remotely accelerates apoptosis in uninfected bystanders. Functionally, recombinant GDF15 increases BCL2L13 and apoptosis, while genetic dampening of BCL2L13 blunts Omicron-specific high-intensity bystander death. In clinical samples, plasma GDF15 associates with mortality, SOFA scores, and lower lymphocyte counts, bridging the epithelial–immune axis to patient outcomes. Our data delineate a two-track model of Omicron immune injury—CD63-enabled T-cell entry plus GDF15–BCL2L13-driven bystander apoptosis—that reconciles lower epithelial cytopathicity with deeper T-cell depletion in critical disease. These findings nominate the GDF15–BCL2L13 axis as a mechanistic marker and potential point of intervention.

Small extracellular vesicles (sEVs) are particles secreted from cells that play vital roles both in normal physiology and in human disease. sEVs are highly enriched in tetraspanin proteins, such as CD...

Severe Omicron cases present profound lymphocytopenia, suggesting variant-specific immune injury. We identify CD63 as a conserved T-cell host factor supporting ACE2-independent SARS-CoV-2 entry. Despite lower intracellular viral loads than the ancestral strain, Omicron elicits enhanced T-cell apoptosis largely through a bystander mechanism. Omicron-stimulated epithelial cells secrete GDF15, which upregulates the pro-apoptotic protein BCL2L13 in T cells and thereby remotely accelerates apoptosis in uninfected bystanders. Functionally, recombinant GDF15 increases BCL2L13 and apoptosis, while genetic dampening of BCL2L13 blunts Omicron-specific high-intensity bystander death. In clinical samples, plasma GDF15 associates with mortality, SOFA scores, and lower lymphocyte counts, bridging the epithelial–immune axis to patient outcomes. Our data delineate a two-track model of Omicron immune injury—CD63-enabled T-cell entry plus GDF15–BCL2L13-driven bystander apoptosis—that reconciles lower epithelial cytopathicity with deeper T-cell depletion in critical disease. These findings nominate the GDF15–BCL2L13 axis as a mechanistic marker and potential point of intervention.

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Haematopoietic stem cells (HSCs) produce all blood and immune cells throughout life, but ageing progressively impairs their function, generating excessive myeloid and megakaryocyte cells at the expense of lymphocytes. This lineage imbalance contributes to immune decline, chronic inflammation and increased disease susceptibility in the elderly, yet the underlying mechanisms remain poorly understood. Here we show that a specific Meg3+ HSC subset (CD150hiSca1hiCD24hiCD201+CD9+CD63+ long-term HSCs) expands dramatically during ageing and drives this lineage skewing. Using multi-omics profiling, we found that inflammatory signals increase H3K23ac levels in aged Meg3+ HSCs, enhancing PU.1 activity through recruitment of the reader protein TRIM24. This epigenetic mechanism promotes excessive megakaryocyte and myeloid production. Of note, disrupting H3K23ac–TRIM24 interaction in aged HSCs restored balanced lineage output and reduced inflammatory signals. Our findings reveal a key mechanism link

Zhang et al. use live imaging of laser-injured zebrafish microvessels to show that macrophages and neutrophils coordinate staged repair. Early tnfa-associated macrophages drive endothelial re-bridging and debris clearance, while neutrophil-derived CD63+ extracellular vesicles promote a later macrophage transition needed for barrier resealing.