R.S. Pero

TL;DR: The development of an eosinophil-less mouse now permits an unambiguous assessment of a number of human diseases that have been linked to this granulocyte, including allergic diseases, parasite infections, and tumorigenesis.

TL;DR: It is shown that eosinophils elicit the expression of the Th2 chemokines thymus- and activation-regulated chemokine/CCL17 and macrophage-derived chemoksine/ CCL22 in the lung after allergen challenge, and blockade of these Chemokines inhibited the recruitment of effector T cells.

TL;DR: It is demonstrated that the infiltration of tumors by eosinophils is an early and persistent response that is spatial‐restricted, suggesting that eos inophils are part of an early inflammatory reaction at the site of tumorigenesis.

TL;DR: An allergen-naive double transgenic mouse model that expresses IL-5 systemically from mature T cells and eotaxin-2 locally from lung epithelial cells is developed, demonstrating that these pathologies are a consequence of one or more eosinophil effector functions.

TL;DR: The development of eoCRE mice represents a milestone in studies of eosinophil biology, permitting eos inophil‐specific gene targeting and overexpression in the mouse as part of next‐generation studies attempting to define eosInophil effector functions.