Browse our latest Immunology and Inflammation articles

Without using control cohorts, a statistical method identifies candidates for immune receptors associated with diseases from repertoire sequencing datasets.

The bZIP transcription factor C/EBPδ enhances expression both of selectin ligands and the chemokine receptor CCR6 on human mucosal-associated invariant T cells, supporting their efficient extravasation into inflamed tissue.

The acquisition of cytotoxic function by human CD4 T cells is an integral part of the T helper 1 differentiation pathway and is limited by the transcription factor ThPOK.

Computer simulations of the evolution of broadly neutralizing antibodies against HIV suggest that non-traditional pathways involving framework mutations which lead initially to increased antibody flexibility do occur, but can be avoided by appropriate vaccine design.

The strength of Toll-like receptor signalling depends on the number and size of MyDDosomes formed as well as on how quickly these structures assemble.

A comprehensive analysis of the glucocorticoid-sensitive pro-inflammatory genes in macrophages reveals fundamental differences between the temporal events and components of transcriptional machinery that the glucocorticoid receptor targets to repress their transcription.

Pre-neoplastic cells in the brain release SDF1, which mediates an immediate infiltration of macrophages that differentiate into microglia-like cells and promote proliferation of pre-neoplastic cells.

Antitumor (natural killer) NK cell responses are negatively regulated by interactions between NK cells and endogenous NKG2D ligands constitutively expressed on lymph node endothelial cells and super-induced on tumor-associated endothelium.

To quantify serum or antibody activity against HIV-1, logistic regression of single-dilution neutralization outcomes can efficiently summarize neutralization potency and indicate which samples may lack sufficient statistical support, for high-throughput screening in large-scale vaccine trials.

Intersectin2 deficiency is associated with impaired humoral responses to viral infection and B-cell-intrisic defects in germinal centre formation, resulting from the reduced ability of intersectin2-KO B cells to establish cognate interactions with helper T cells.