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Latent gammaherpesvirus infection predisposes mice to develop more severe disease following induction of arthritis by elevating pathogenic interferon-gamma-expressing age-associated B cells.

A mouse model supports the hypothesis that latent Epstein–Barr virus exacerbates the symptoms of rheumatoid arthritis.

Immature CD10^neg neutrophils and CD14⁺HLA-DR^neg/low monocytes inducing proinflammatory and adaptive immune responses emerge in patients with large acute myocardial infarction.

Endoplasmic reticulum-associated degradation (ERAD) is a critical protein quality control checkpoint for thymocyte β-slection.

RTN3 is upregulated upon RNA viral infection, in turn suppresses antiviral responses by impairing TRIM25-mediated RIG-I K63-linked polyubiquitination and decreases neutrophil populations and inflammatory infiltration, representing a novel inflammatory resolution.

Neutrophil swarms form around a single endogenous pioneer neutrophil in vivo, mediated by DNA release from pioneer neutrophils.

Alternative first exon usage was the major event observed in macrophages during inflammation, which resulted in the elucidation of a novel isoform and regulatory mechanism of the protein-coding gene, Aim2.

Peptidomics method development and analysis of qualitative differences of peptide patterns in human wound fluids provide potential biomarkers for wound healing and infection.

Soluble Fas ligand interacts specifically with tumor necrosis factor receptor superfamily (TNFRSF)10B, also known as death receptor 5, exacerbating arthritis in a Fas-independent manner.

Repression of type I interferons by SP140 is essential for resistance to Legionella pneumophila and Mycobacterium tuberculosis.