Browse our latest Immunology and Inflammation articles

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.

Imaging mass cytometry simultaneously lights up distinct immune cells in the brain.

Toxoplasma gondii infection leads to conversion of natural killer cells into cells resembling innate lymphoid cells, group 1, that circulate widely, disrupting current notions suggesting that these cells have distinct lineages.

Microbial-sensing TLRs drive responses to the microbiota, while nucleic-acid sensing TLRs control responses to endogenous ligands, revealing novel regulation of B-1a responses through integrated BCR/TLR mediated activation.

B-1 cell unresponsiveness to antigen-stimulation is overcome during infections when Toll-like receptor engagement removes negative regulators of B cell receptor signaling, thereby supporting B-1 cell differentiation to IgM-secreting plasmablasts.