Browse our latest Immunology and Inflammation articles

High-throughput sequencing of the memory T cell receptor repertoire and machine learning can predict robust antibody and CD4 T cell response to de novo hepatitis B vaccine.

Granzyme A^-/- mice, which have contributed to a body of research into this enzyme, emerge to have a mixed C57BL/6J-C57BL/6N genetic background, compromising our understanding of granzyme A and highlighting a widespread problem for knockout mouse studies generally.

KLK10 is a flow-sensitive endothelial protein that serves as an anti-inflammatory, barrier-protective, and anti-atherogenic factor with therapeutic potential.

Fluorescent protein-based reporter mouse models revealed that thymic cooperative antigen transfer is mediated by preferential pairing between a particular thymic epithelial cell subset and specific subset(s) of thymic dendritic cells.

METTL3 and m6A modifications could alleviate endothelial activation and atherogenesis through accelerated degradation of oscillatory flow-induced EGFR mRNA expression.

Sorting nexin 9, a membrane curvature inducing protein, creates a distinct environment within clusters of the co-receptor CD28 and thereby allows T cell activation to proceed to a successful outcome.

Patients with different rs1990760 variants have a differential inflammatory response to severe SARS-CoV-2 infections, so that those with a TT genotype have an attenuated systemic inflammation and may not benefit from steroid therapy.

Prevaccination levels of transcriptional modules related to monocytes, dendritic cells, and other immune categories correlate with clinical malaria risk in RTS,S/AS01E-vaccinated African children, suggesting that certain monocyte subsets may inhibit RTS,S/AS01E-induced protective responses.

Only three Spike mutations enable murine SARS-CoV-2 infection, which is still strictly ACE2 dependent and causes a COVID-19-like disease in mice with immunopathology-driven lung damage.

The spike protein of SARS-CoV-2 triggers macrophages and epithelial cells to produce excess levels of pro-inflammatory molecules, which can do more harm than good.