Browse our latest Immunology and Inflammation articles

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.

Deep learning improves estimation of T cell receptor cohort frequencies and learns the rules of VDJ recombination, potentially making it helpful for vaccine design.

B cells regulate production of neutrophils by a novel mechanism by releasing ST6Gal-1, an active sialyltransferase, that suppresses granulopoiesis.

A single-nucleotide I232T polymorphic change in FcγRIIB's transmembrane domain bends FcγRIIB's ectodomains toward cell membrane to allosterically hinder FcγRIIB's ligand association, providing novel molecular mechanism for functional loss of FcγRIIB-I232T.