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Cell Biology, Neuroscience and Physiology Program
B.S. 2012, William Paterson University, Wayne, NJ
Thesis Advisor: Theresa L. Chang, PhD
Department of Microbiology, Biochemistry and Molecular Genetics
Monday, December 11, 2017
12:00 PM, ICPH 1st Floor Auditorium
InterferonƒÕ (IFNƒÕ) is a type I IFN with distinct gene and protein expression characteristics from other type I IFNs such as IFNƒÑ/ƒÒ. Unlike IFNƒÑ/ƒÒ, IFNƒÕ is not induced by Toll-like receptors or interferon regulatory factors (IRFs) -3, -5, or -7. Rather, IFNƒÕ is constitutively expressed in the epithelium of mucosal tissues including the female reproductive tract (FRT). IFNƒÕ gene expression can be modulated by estrogen, seminal plasma, and TNFƒÑ. While IFNƒÕ has less potent antiviral responses than IFNƒÑ, it protects primary macrophages against human immunodeficiency virus and mice against infection by herpes simplex virus-2 and Chlamydia. This work aims to gain a better understanding of gene and protein expression of IFNƒÕ in the human cervical epithelium of the FRT. We demonstrated the expression and secretion of glycosylated bioactive IFNƒÕ proteins in a mammalian expression system, the Expi293 cell line but not HEK 293T cells, by using the native signal sequence. Primary human cervical cells endogenously expressed IFNƒÕ proteins that were localized mainly in the perinuclear space and partially in the Golgi apparatus. Immunostaining analysis of the IFN𝜀 expression in cervical tissues revealed that IFNƒÕ proteins were present most abundantly in the glandular and luminal cervical epithelium. Some IFNƒÕ proteins were also detected in the stroma. Finally, the differential effects of mucosal cytokines on IFNƒÕ, IFNƒÑ, or IFNƒÒ gene expression in an endocervical cell line and primary cervical cells were investigated. We found that IFN𝜀 gene expression was induced by TNFƒÑ and IL-1£]. Additionally, TNF⍺ activated the IFNƒÕ promoter through the NFƒÛB signaling pathway. In sum, this study offers a better insight into the biology of IFN𝜀 expression and regulation in the epithelium of the FRT.