Browse our latest Immunology and Inflammation articles

Fibroblast growth factor 21 blocks hepatic lipid influx and accumulation, prevents Kupffer cell activation, and inhibits the formation of hepatic lipid- and scar-associated macrophages, thereby likely inhibiting fibrogenesis in nonalcoholic steatohepatitis in humanized APOE*3-Leiden.CETP mice.

Human leukocyte antigen class I (HLA class I) polymorphisms dictate the degree of endo-lysosomal assembly, which can supplement endoplasmic reticulum assembly for constitutive HLA class I expression and increase the efficiency of cross-presentation.

Early IFN-I response dynamics are initiated in only fractions of cells, of which their epigenetic profile is transiently heritable and subject to the effects of quorum sensing.

The expression of DECTIN-2 family C-type lectin receptors on macrophages and monocytes is inhibited by the Th2 cytokine IL-4, which suggests a mechanism for inhibition of Th17 responses to MINCLE-dependent vaccination responses by underlying helminth infection.

A hallmark property of non-functional clonotypes was used to develop a universal and fully computational method for detection and correction of multiplex PCR-specific quantitative bias in adaptive immune receptor repertoire.

Integrated single-cell and spatial genomics provides the first molecular map of the human oral mucosa and reveals a novel pro-inflammatory fibroblast involved in disease progression.

Maternal obesity and high-fat diet present metabolic, signaling, and epigenetic impediments to pathogen recognition in fetal innate immune cells that result in a state of immune paralysis during gestation and at birth.

By comparing different subsets in mouse inducible Tfh (iTfh) cells and human circulating Tfh (cTfh) cells after vaccination, Tfh17 cells were found to be better than Tfh1 or Tfh2 cells in maintenance and support immunological memory of humoral immunity.

Flow cytometric analysis of antigen-specific B and T cell responses to heterologous immunization reveals intact dendritic cell function, but selective defects in germinal center formation, in mice with concurrent malaria.

Genetic analyses using a new oral infection mouse model demonstrate that cell death pathways protect against the gastrointestinal bacterial pathogen Shigella flexneri.