Signaling
Cytokines, chemokines, degranulation triggers, and the receptor biology that drives granulocyte activation, recruitment, and resolution.
Kouro and Takatsu review IL-5 and its receptor as the central axis of eosinophil production and survival.
Jose et al. discovery of eotaxin as a selective eosinophil chemoattractant.
Ley et al. review of capture, rolling, arrest, crawling, and transmigration.
Segal review of the NADPH oxidase and how the phagocytic vacuole kills microbes.
Li et al. PAD4-deficient neutrophils cannot form NETs, and the mice are more susceptible to bacterial infection.
Kraft and Kinet review of the high-affinity IgE receptor and its signaling in basophils and mast cells.
Iwasaki and Akashi map the progenitor steps from stem cell to granulocyte lineages.
Sokol et al. basophils respond to a protease allergen and help initiate Th2 responses in mice.
Hayashi et al. human neutrophils express functional TLRs that modulate their responses.
Hogan et al. on single-cell profiling of granulocytes in atopic disease.
Almas et al. review of eosinophil granule release routes, including piecemeal degranulation.
Koenis et al. report that erythroblast lipid mediators shape neutrophil development; single study.
Xu et al. review how mitochondrial reprogramming shapes NETs in COPD and asthma.
Shin et al. show that viral-pattern-activated nasal fibroblasts secrete chemokines that recruit eosinophils in chronic rhinosinusitis with nasal polyps.
Suzuki et al. show that monomeric hapten terminates IgE-triggered calcium entry by breaking the STIM1-Orai1 channel complex in basophil-like cells; early mechanistic data.
Case report: positive basophil activation test (BAT) with sevoflurane in a patient with repeated perioperative reactions; demonstrates BAT utility for volatile anaesthetic allergy.
Review: NETs are web-like DNA-histone-granule protein structures released by activated neutrophils; play host defense and pathological roles in bacterial infections. Discusses mechanisms and therapeutic targeting strategies.
Fibrin deposits drive NETosis; platelet GPVI receptor is the upstream signal. Hyperglycemia exacerbates the pathway independently of diabetes diagnosis. Mechanistic study.
Type I interferon receptor (IFNAR1) drives a conserved iron homeostasis circuit that sustains neutrophil pathogenicity across mucosal tissues; single-cell transcriptomics and CRISPR screen identify mitochondrial iron handling as the downstream mechanism; targeting selectively dampens pathogenic function without compromising antimicrobial activity.