Browse our latest Immunology and Inflammation articles

Genetically engineered, CD73-redirected human NK cells show potent antitumor activity in vivo by impairing adenosinergic activity of CD73 in cancer.

Switches in cell state downstream of pathogen exposure are driven by a deeply conserved disorder-to-order phase transition in an immunity signaling network.

SARS-CoV-2 experienced ocrelizumab-treated MS patients benefit from SARS-CoV-2 mRNA vaccination by inducing broadprotective CD8+ T-cells, whereas methotrexate-treated RA patients induce delayed but strong antibody responses, which support vaccine strategies for these patient groups.

Eutherian CD4 evolved counterbalancing motifs in the extracellular, transmembrane, and intracellular domains that regulate CD4⁺ T cell responses to peptide antigens presented by class II MHC (pMHCII).

Description of the transcriptional and clonal landscape of virus-specific CD4⁺ T cells in acute and chronic viral infections, and a new reference map to interpret CD4 T cell diversity across tissues and biological models.

Transcriptomic and bionergetic analysis shows the importance of HIF-1α activation in enabling tissue-resident alveolar macrophages to perform glycolytic metabolism, which prevents their death and attenuates influenza A virus-induced acute lung injury.

Yeast surface-displayed libraries, when coupled with pooled oligonucleotide synthesis and next-generation sequencing, can be used as a platform to assess binding of whole viral proteomes to class II major histocompatibility complex proteins.

An improved 'plug-and-play' reversed FluoroSpot assay is described and validated that allows the simultaneous assessment of antibody cross-reactivity at the single-cell level against up to four variants of a polymorphic antigen of interest.

A model-based approach for modelling the immune control of viral dynamics is applied to quantify the effect of several SARS-CoV-2 vaccine platforms and to define mechanistic correlates of protection.

Pathological TNF-α-producing B cells are involved in the pathological process of polycystic ovary syndrome, and metformin inhibits mTOR phosphorylation, affects metabolic reprogramming, and further inhibits TNF-α expression in pathological B cells.