Browse our latest Immunology and Inflammation articles

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.

Polarizing susceptibilities to recurrent bladder infection are shaped by a duality in TNFɑ-mediated inflammation dynamics upon challenge infection that is dictated by the outcome of the initial infection.

Blood flow-driven shear forces guide the sequential signaling of two antagonistic paired receptors, a critical bi-facet step that first supports leukocyte docking, then initiates transmigration through endothelium.

Uncovering a mechanism for how inflammatory signaling is opposed by a phosphatase identifies a potential druggable target to treat E. coli sepsis.

Inflammatory dynamics are tailored to bacterial class through macrophage integration of microbial stimuli and cytokine feedback.

Systemic inflammation is greater in individuals with concurrent TB and diabetes than in euglycemic individuals with TB, and this disparity persists through the full 6-month course of anti-tubercular treatment.

The ubiquitin ligase c-Cbl preferentially targets unique-region phosphorylated LynA for rapid degradation, regulating its expression and differentially tuning signaling responsiveness in macrophages and mast cells.