"The University Scholars program offered the unique experience of working together with some of the best researchers in the world, while completing a jointly designed research project, which was rather appealing to me. After my initial exposure to research in Dr.Wallet’s lab dealing with oral immunity homeostasis, I was intrigued with the objectives of her lab. The University Scholars program afforded me the ability to interact with Dr.Wallet in a mentoring capacity while simultaneously completing a research project that satisfied the needs of her lab and my interests. During my time as a University Scholar I plan on acquiring a better understanding of both the scientific and scholarly methods, while gaining hands on experience with a large variety of laboratory techniques to improve my technical repertoire. My goals for this coming academic year are to complete my currently proposed research project, to gain proficiency in several assays and to gain a more detailed understanding of oral immunity."
My current broad research interests are focused on oral immunity homeostasis. In particular, my research concentrates on the innate immune responses of Type 1 diabetic individuals, with an overriding goal in determining a mechanistic action for Type 1 diabetes.
Academic and Other Awards
- UF Price Scholarship
- Vivian M. Johnson Scholarship
- St. Petersburg Sungoddess Scholarship
- Pre-Dental ASDA
- Pre-Dental Society
- Recreational Sports Board of Directors
- Alpha Epsilon Delta
- J. Wayne Reitz Union Board of Directors Mortar Board
I currently do volunteer work in the University of Florida College of Dentistry in various dental clinics. I also volunteer for Hospice, All Children's Hospital and Ronald McDonald House.
Hobbies and Interests
- Running, playing tennis, going to the gym, reading, cooking, baking, and traveling.
Characterization of Regulation of TLR2 Induced Homeostasis in Oral Epithelial Cells
It has been postulated that in Type 1 Diabetes (T1D) alterations in mucosal barrier function and mucosal immunity are implicated in disease pathogenesis.Data demonstrate that TLR-induced hyper inflammatory activation of oral mucosal epithelial from T1D patients concomitant with absence of TLR2-induced homeostasis. Also,exposure of oral epithelial cells to hyperglycemia,blocks TLR2-induced regulatory responses and exacerbates the pro-inflammatory response.This data indicates that both T1D intrinsic epithelial cell defects can disrupt mucosal homeostasis.Thus it’s imperative to identify the mechanism of TLR2-induced homeostasis in primary human oral epithelium along with the identification of regulatory mechanisms involving TLR signaling intermediates.We hypothesize that during TLR2 ligation a different pattern of signaling inhibitors will be expressed in human epithelial cells derived from T1D individuals(dHOK) compared to HOK derived from non-diabetes prone individuals allowing for activation of inflammation. HOK and dHOK will be isolated from gingival biopsies taken during third molar extractions. Cells will either be left untreated or stimulated with ultra-pureTLR2,TLR2/1,TLR2/6 or TLR4 agonists.Innate immune phenotype profiles will be evaluated 3 and 6 hours post-stimulation by measuring secreted IL6 and IL8(inflammation),and IL10 and TGFβ1,2,3(homeostasis) simultaneously using Milliplex® technology. In all simulation assays,the expression of toll like receptor signaling inhibitors [IRAK-M,SOCS-1,A20 and TOLLIP]will be evaluated by Western Blot.Protein complexes will be resolved on an SDS-PAGE gel,transferred and probed with TLR–specific,HRP-tagged antibodies for TLR1,TLR2,TLR4,and TLR6.To quantify signaling inhibitor protein expression,cell lysates will be immunoprecipitated with either anti-hTLR4,antil-hTLR2,anti-hTLR1 or anti-hTLR6 and Dynabeads,Protein G. We expect that there will be disruption of signaling inhibitor expression profiles in TLR2-activated gHOK,preventing TLR2 homeostatic outcomes.We also expect to identify unique TLR2-induced expression profiles in HOK from non-diabetic patients when compared to TLR2/1 or TLR2/6 activation of HOK.The data generated from these experiments will allow us to evaluate the relative contribution of each regulatory mechanism observed alone as well as in combination with others.