When:
Friday, May 25, 2018
12:00 PM - 1:00 PM CT
Where: Prentice Women's Hospital, 3rd Floor, Canning Auditorium, 250 E. Superior, Chicago, IL 60611 map it
Audience: Faculty/Staff - Student - Public - Post Docs/Docs - Graduate Students
Contact:
Barb Crenshaw
Group: Medicine - Allergy/Immunology
Category: Academic
Speaker
Steven J Ackerman, PhD
University of Illinoic at Chicago (UIC)
Research Interests
Transcriptional regulation of hematopoietic (myeloid) development and granulocyte (eosinophil) lineage-specific gene expression. Molecular biology, structural biology (structure-function relationships) and biologic activities of eosinophil-derived enzymes (phospholipases, lysophospholipases), granule cationic proteins/cytotoxins, and galectins as mediators of eosinophil effector function in allergic inflammation, tissue damage and disease pathogenesis. Eosinophil effector functions in inflammation, tissue remodeling, and fibrosis in asthma, allergy, and other eosinophil-associated diseases.
Our research interests center on the molecular biology, biochemistry and hematopoietic development of the human eosinophil leukocyte in health and disease pathogenesis. Ongoing research projects focus on the: (1) transcriptional mechanisms that regulate eosinophil development and lineage-specific gene expression in the process of commitment and terminal differentiation of multipotential myeloid progenitors to the eosinophil lineage, (2) molecular biology, biochemistry and biologic actions of granule and cytosolic enzymes and cationic cytotoxins expressed by eosinophils, and their roles in the effector functions of this granulocyte in disease pathogenesis, (3) structural biology (structure-activity relationships) of eosinophil granule-associated cytotoxins and enzyme mediators of inflammation, (4) cytokine regulation and mechanisms of eosinophil terminal differentiation, activation and secretion, including cytokine-activated signal transduction pathways, and (5) the roles of eosinophils and their mediators in normal tissue remodeling and pathological tissue fibrosis.