Browse our latest Immunology and Inflammation articles

A novel mutation in SCGN is associated with risk for inflammatory bowel disease and implicates the intestinal neuroendocrine compartment in the pathogenesis of this disorder.

A membrane-associated, supramolecular protein complex with dynamically changing components, the central supramolecular activation cluster, regulates the generation of the T cell effector cytokine IL-2 depending on its composition.

Mycobacterium tuberculosis exploits an IFN/IL6/CEBP axis linked to monocyte expansion in humans.

Virus infection in mosquitoes initiates a highly discriminatory process in which fragments of viral RNA are reverse transcribed to create DNA copies that serve as templates of small antiviral RNAs.

Natural Tr1-like cells do not form a functionally stable memory response to allergens, and this instability may limit efforts to re-establish tolerance by expanding Tr1.

The complement pathway can contribute to corneal sensation loss and nerve damage during ocular surface inflammation.

Interactions between T helper cells and the complement system promote loss of sensory neurons in the eye.

Impairment of the autocrine S1PR1-Gi signaling on HEVs results in high-endothelial cell apoptosis, reduced CCL21-secretion from HEVs, and cessation of HEV-DC interactions and lymphocyte immigration across the high-endothelial barrier.

Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na⁺) channels.

TCR and CD40L microclusters are linked in synaptic ectosomes (extracellular vesicles) and released in the immunological synapse by helper T cells and induce dendritic cell maturation and cytokine production.