Browse our latest Immunology and Inflammation articles

Cell-free DNA methylation markers allow monitoring of immune and inflammatory cell turnover.

Electron paramagnetic resonance spectroscopy quantitatively correlates structural damages of serum albumin with COVID-19 severity and mortality thus suggesting albumin replacement therapy as a strategy to rescue patients at risk of mortality.

Histone deacetylase 3 is required for CD4+ T cells to downregulate two cholesterol efflux transport proteins, ABCA1 and ABCG1, for successful proliferation after antigenic stimulation.

Single-cell analysis revealed that autoantigen-reactive B cells changed the type of cytokines they produced from anti-inflammatory IL-10 and IL-35 to pro-inflammatory IL-6 and IL-23 as affinity to autoantigen increased.

By fusing influenza viral conserved epitopes and a superantigen fragment, we constructed a recombinant protein that might be a candidate universal broad-spectrum vaccine for the prevention and treatment of multiple influenza viruses.

Functional characterization of the alpha/B1.1.7 SARS-CoV-2 variant revealed an eightfold affinity increase of the N501Y RBD to human ACE-2 and that even a low inoculation dose of the alpha variant induces severe disease and fast progression in transgenic hACE2 mice.

Distance-based TCR analysis enables grouping of biochemically similar clonotypes into meta-clonotypes that have increased publicity, and therefore statistical power, for population-level detection of antigen-specific T cells in infection and vaccination.

Immuno-affinity enrichment combined with liquid chromatography-mass spectrometry can be used to detect viral proteins to confirm the presence of SARS-CoV-2 in clinical samples.

A high-throughput mitochondrial phenotyping approach quantifies mitochondrial features among purified human immune cell subtypes and provides foundational knowledge to map inter- and intra-individual variation in mitochondrial energetics with high biological specificity.

The pathogenic success of Mycobacterium tuberculosis relies in part on its ability to blunt a component of the TLR2-dependent immune response.