Julie Ledford

Photo of Julie Ledford

Julie Ledford

Associate Professor, Cellular and Molecular Medicine
Associate Professor, Immunobiology
Associate Professor, Medicine
Associate Professor, Clinical Translational Sciences
Associate Professor, Applied BioSciences - GIDP
Member of the Graduate Faculty
Associate Professor, BIO5 Institute
Primary Department
Cellular & Molecular Medicine
Department Affiliations
Medicine
Cellular & Molecular Medicine
BIO5 Institute
Contact
(520) 626-0276
jledford@arizona.edu

Work Summary

Julie Ledford's research focuses on respiratory disease, and genetic and molecular mechanisms of allergic airway diseases in children.

Research Interest

Dr. Ledford’s current work in the area of pulmonary surfactant immunobiology combines her knowledge of mouse genetics, pulmonary disease models and immune function regulation and focuses on understanding the role of Surfactant Protein-A (SP-A) and how it regulates signaling pathways within various immune cell populations. Specifically, she is interested in how SP-A regulates degranulation, either directly or indirectly, of two important cell types in asthma: mast cells and eosinophils. More recently, Dr. Ledford’s research has focused on understanding how genetic variation within human SP-A2 alters functionality of the protein in relation to eosinophil activities and how this translates to characteristics observed in human asthma.

Publications

Takezaki, A., Kitamura, A., Setoguchi, Y., Itoh, Y., Ledford, J., Goto, H., Nishioka, Y., & Yasutomo, K. (2017). Notch-mediated necroptosis due to a mutation in SFTPA1 is a crucial driver for pulmonary fibrosis.. Nature Immunology.
Ledford, J. G., Addison, K. J., Foster, M. W., & Que, L. G. (2014). Eosinophil-associated lung diseases. A cry for surfactant proteins A and D help?. American journal of respiratory cell and molecular biology, 51(5), 604-14.

Surfactant proteins (SP)-A and SP-D (SP-A/-D) play important roles in numerous eosinophil-dominated diseases, including asthma, allergic bronchopulmonary aspergillosis, and allergic rhinitis. In these settings, SP-A/-D have been shown to modulate eosinophil chemotaxis, inhibit eosinophil mediator release, and mediate macrophage clearance of apoptotic eosinophils. Dysregulation of SP-A/-D function in eosinophil-dominated diseases is also not uncommon. Alterations in serum SP-A/-D levels are associated with disease severity in allergic rhinitis and chronic obstructive pulmonary disease. Furthermore, oligimerization of SP-A/-D, necessary for their proper function, can be perturbed by reactive nitrogen species, which are increased in eosinophilic disease. In this review, we highlight the associations of eosinophilic lung diseases with SP-A and SP-D levels and functions.

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