Browse our latest Immunology and Inflammation articles

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.

Highly specific gene manipulation in mouse thymic epithelial cells (TECs) shows that fine-tuning of β-catenin expression is required for TECs to generate an optimal thymic microenvironment to support T-cell development.

Binding of the translation initiation factor eIF3 to the messenger RNAs encoding the T cell receptor subunits alpha and beta is required to drive a short burst in their translation and promote a strong T cell response.

Infection with Mycobacterium tuberculosis triggers de novo synthesis of polyunsaturated fatty acids by host macrophages, which promote their antimicrobial responses but feed the intracellular pathogen.

In depth phenotyping from tissues and in vitro activation studies reveal antiviral function of MAIT cells- with particular emphasis on HIV infection.

Influenza vaccination in humans stimulates novel B cell evolution that is detectable in germinal centers, but not the peripheral blood.

A mouse model of inducible inflammasome activation in intestinal epithelial cells reveals separate inflammasome-dependent and -independent cross-presentation pathways for epithelial cell-derived antigen.

Recognition of SARS-CoV-2 spike protein by innate immune sensor TLR2 leads to the induction of inflammatory mediators and constitutes a mechanism for cytokine storm during COVID-19.

Deficiency of capicua, a transcription factor that suppresses autoimmunity, impairs positive and negative selection processes by attenuating TCR signaling in CD4⁺CD8⁺ double-positive thymocytes.