Browse our latest Immunology and Inflammation articles

Indoxyl sulfate, a key uremic toxin in chronic kidney disease (CKD), induces trained immunity in monocytes via crosstalk between aryl hydrocarbon receptor (AhR)-dependent epigenetic reprogramming by enhancement of the arachidonic acid pathway and AhR-independent metabolic rewiring.

Cancer cell antigen presentation, a requirement for immune-mediated tumor rejection, is induced by dihydroorotate dehydrogenase-inhibitor-mediated cancer cell pyrimidine nucleotide depletion via P-TEFb-dependent transcriptional upregulation of MHC-I and related genes.

The role of lysosomal Ca²⁺ flux associated with K⁺ efflux, a well-known event in inflammasome activation in metabolic inflammation and inflammasome activation, has been presented.

Interferon contributes to photosensitivity at least in part by causing Langerhans cell ADAM17 dysfunction, raising the possibility that anifrolumab ameliorates lupus skin disease in part by restoring Langerhans cell function.

A gene expression data-informed model reveals that a small fraction of interferon-producing cells can effectively constrain early virus spread in epithelial tissue, elucidating connections between critical dynamics and infection heterogeneity.

A newly identified immunometabolic mechanism clarifies the aberrant trafficking of dendritic cells to lymph nodes in tuberculosis.

Severely immunodeficient B2m-NOG mice transplanted with human peripheral blood mononuclear cells from multiple sclerosis patients partially reproduce disease immunopathology and represent novel experimental models for studying human immune responses to the central nervous system in a rapid and personalized manner.

The pseudokinase Tribbles1 is expressed in human monocytes after mycobacterial challenge and can be manipulated to be host protective against mycobacterial infection, due to control of innate immune cell function, in a zebrafish tuberculosis model.

Enigmatic long-lived plasma cells display an enhanced clustering in bone marrow niches and require CXCR4 for retention, survival, and maintenance of antibody titers.

Genetic engineering of murine myeloid cells reveals the challenges in ectopic expression of chemiric receptors and provides a novel framework to endow them with tumor-specific cytotoxic ability.