Browse our latest Immunology and Inflammation articles

Pathogen-specific CTLs are programmed to provide customized responses against infection, by inflammatory molecules that promote localization in peripheral and lymphoid tissues using alternative signaling mechanisms.

Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.

Th2 cell heterogeneity was revealed by combined transcriptome and T-cell receptor sequencing of single Th2 cells from lung and lymph node of helminth-infected mice and led to identification of a helminth-specific T-cell receptor.

The IgG4 subclass, previously considered anti-inflammatory due to its weak effector function, could either reduce or exacerbate autoantibody pathogenicity in the context of different IgG4-mediated autoimmune diseases.

Glutamine deprivation reprograms chondrocytes, attenuates inflammation, and such intervention may be protective against joint inflammation.

Extracellular vesicles derived from natural killer cells contain a specific repertoire of microRNAs that promote Th1 responses.

By binding with their type 1 pili to the cell surface receptor CD14, pathogenic E. coli suppress the capacity of dendritic cells to activate T cells.

Cross-reactive T cell immunity against the SARS-CoV-2 is severely compromised in HIV viremic individual.

Naive CD4 and CD8 T cells in mice increase their survival capacity with age, but their numbers are not homeostatically regulated.

Mathematical models encoding biological hypotheses reveal new insight into the dynamics of naive immune cells in mice from birth to old age.