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Eosinophils are granulocytes – with granules that are stainable by eosin – that develop during haematopoiesis in the bone marrow before entering the blood. Through the release of their cytotoxic granule cationic proteins, eosinophils contribute to defence against parasites and other infections. They also contribute to asthma pathogenesis and allergy responses.
Eosinophilic esophagitis (EoE) is a chronic inflammatory disease of the esophagus with unclear immune cell involvement. Here the authors generate a single cell transcriptomic dataset with 400k cells from the esophageal mucosa of active EoE patients, remission EoE patients, and healthy individuals to characterise esophageal cellular composition, phenotype and interaction in this disease.
Eosinophils are innate immune cells critical for protection from parasites, but their developmental origin remains under studied. Here they analyze development of eosinophils in zebrafish and find that eosinophilic lineage commitment and differentiation are regulated by the Cebp1-Cebpβ axis.
Single-cell transcriptomic profiling and functional assays are used to identify subpopulations of eosinophils that are present in the mouse gastrointestinal tract and provide insight into the role of these cells in inflammatory bowel diseases in humans.
The role of eosinophils in response to cancer is not well understood. Here the authors document evidence that eosinophils contribute to the immune response to cancer and to immunotherapies and postulate that these cells might be more important than expected in these contexts.
Blood eosinophil (EOS) counts may serve as risk factors for human coronary heart diseases. Here the authors show that increased circulating and myocardial EOS after myocardial infarction play a cardioprotective role by reducing cardiomyocyte death, cardiac fibroblast activation and fibrosis, and endothelium activation-mediated inflammatory cell accumulation.
Immune cells are important regulators of adipose tissue function, including adaptive thermogenesis. Here the authors show that mice with Krüppel-like factor 3 (KLF3) deficiency in bone marrow-derived cells have increased adipose tissue beiging which may at least in part be due to altered eosinophil paracrine signaling.
In breast cancer, an effective response to therapy with immune checkpoint blockade depends on T cell–eosinophil collaboration: CD4+ T cells produce IL-5 to mobilize eosinophils, which in turn help to activate antitumour CD8+ T cell responses.
This study describes a mechanism of tumour immune evasion through post-translational chemokine modification by dipeptidyl peptidase 4, which inhibits eosinophil-mediated antitumour responses.
Combined immunotherapy using checkpoint blockade (anti-CTLA4 and anti-PD-1) and the DPP4 inhibitor sitagliptin reveals the existence of a T cell– and eosinophil-targeted immunotherapy approach for solid tumors.
