TH2 Cytokines Can Induce STAT5 Activation in Murine Eosinophils

Abstract

By Abigail Vossler, Biological Sciences

Advisor: Patricia Fulkerson

Presentation ID: PM_D16

Abstract: Janus kinase and signal transducer and activator of transcription (JAK-STAT) pathways are critical in the eosinophil (Eos) intracellular signaling. The JAK-STAT pathway is activated when a receptor associated JAK phosphorylates an inactive STAT. The phosphorylated STAT's (pSTAT) then dimerize and translocate to the nucleus where they bind transcription factors and increase the transcription of target genes. STAT5 is expressed by mature eosinophils and has been associated with the transcription of genes that affect eosinophil growth, differentiation, and chemotaxis. Studies have shown that GM-CSF, a white blood cell growth factor, can cause P-STAT5 in other cell types such as in macrophages etc. This study was designed to investigate whether GM-CSF can cause phosphorylation of STAT5 (P-STAT5) in cultured murine eosinophils. The overall goal of this study is to understand GMCSF mediated effects on eosinophil development and transcriptome. For our study we used murine eosinophils that were cultured from the bone marrow in presence of IL-5. We hypothesized that GMCSF would lead to pSTAT5. A complete understanding of STAT signaling could assist in developing therapy for a wide variety of eosinophil related diseases such as eosinophilic asthma, eosinophilic esophagitis, or Job's syndrome.