Proliferation, Plasticity, and Migration: Exploring the synergistic relationship between eosinophils and TH2 cells in development of HES-like syndrome

Abstract Aberrancies in eosinophil proliferation, activation and chemotaxis can lead to acute eosinophilic leukemia, paraneoplastic eosinophilia associated with T cell lymphoma carcinomas, Hypereosinophilic Syndrome (HES), respectively. HES is an idiopathic disease affecting humans veterinary patients characterized by persistent (>1,500 cells/uL) infiltration of solid organs leading increased morbidity mortality. Previous studies have demonstrated the role NF-κB inducing kinase, NIK, upstream regulator noncanonical signaling pathway, development a HES-like syndrome due aberrant TH2 polarization Nik−/−murine model. However, intricacies granulopoiesis, eosinophil/neutrophil plasticity, chemotactic ability has not been assessed during Nik−/−mice. Here we show that loss NIK potentially enhances CCL11, eosinophilic/neutrophilic affects granulopoiesis bone marrow spleen beginning at level metamyelocytes, despite decreasing proliferative potential these cells. Taken together, results suggest pathway plays dictating hematopoietic eosinophils highlights synergistic relationship cells their respective cytokines Overall, findings warrant further study better characterize described above understand diseases. Virginia-Maryland College Veterinary Medicine Institute for Critical Technology Applied Science