Mentor: Dr. Joseph Larkin III
College of Agricultural and Life Sciences
"I always heard about research from when I was growing up as a child, and decided to further explore this field in high school where I interned with the United States Department of Agriculture in a biochemistry lab and truly enjoyed the experience and the thought process that came with it. I decided to continue involving myself in research here at UF in the lab of Dr. Joseph Larkin III. However, I have also attempted to give myself exposure to other potential career paths including jobs in agricultural sciences through my course work and the field of medicine through physician shadowing and clinical volunteering. Although all of these areas are very important and interesting, I see no better fit for me than in a research based setting in an area such as immunology. I am grateful to be working in a lab with a very supportive environment and under a mentor that prioritizes my best interests for the present and future. My mentor has also allowed me to grow into my own research project where I am able to critically think about the problem I am faced with, pose possible solutions, and then apply these solutions. This has lead me to become very excited to hopefully move into a suitable PhD program in immunology next year."
Microbiology and Cell Science
Agricultural and Natural Resource Law
- SOCS1 Deficiency
- Lupus Pathologies
- Shands Arts in Medicine
- DuMond Conservancy
- Habitat for Humanity
Hobbies and Interests
Dysregulation of Leukocytes, Mediated by SOCS1 Deficiency, is Correlated to Skin Pathology and other Ailments: Implications for Therapeutic Targeting
Although dysregulated immune cell activation and cytokine signaling are known to contribute to autoimmune disease, ways to target and prevent these anomalies are limited. Notably, an intracellular protein, Suppressor of Cytokine Signaling-1 (SOCS1) is important in the regulation of both immune cell activation and cytokine signaling. Mice lacking expression of SOCS1 (SOCS1-/-) exhibit dysregulated immune function characterized by enhanced pro-inflammatory cytokine production and significantly decreased lifespan. Our lab has demonstrated that treating these mice with a peptide that mimics SOCS1 function, SOCS1-KIR, significantly improved survival. One regulatory mechanism by which SOCS1-KIR extended survival of SOCS1-/- mice is through the down regulation of interferon-gamma (IFNg) production. To further investigate the role of IFNg in this process, SOCS1 x IFNg knockout mice were studied. In comparison to SOCS1-/- mice, SOCS1-/- IFNg-/- mice do not develop lethal inflammatory disease. Notably, however, SOCS1-/+ IFNg-/- mice display dysregulated immune function in the form of skin pathologies, and dysregulated IL-17 and IL-2 cytokine production. Preliminary hematoxylin and eosin (H&E) stains of skin pathologies reveal increased numbers of neutrophils, mast cells, and eosinophils in the area. The therapeutic potential for SOCS1-KIR to modulate abnormal skin pathologies will be further examined.