miR125a as Molecular Target of Vitamin D Mediated Inhibition of CD4+ T Cell Differentiation into Th17 cells in MRL/lpr Lupus-prone Mice
Date of Award
Biology & Earth Science
Dr. Simon Lawrance
First Committee Member
Dr. Jennifer Bennett
Second Committee Member
Dr. Steffanie Burk
mir-125a, Vitamin D, Systemic Lupus Erythematosus (SLE), CD4+ T Cells, Th17 cells
Biology | Higher Education | Immune System Diseases | Immunopathology | Other Immunology and Infectious Disease | Translational Medical Research
The dynamic function of vitamin D in an array of immunomodulatory and anti-inflammatory mechanisms and its implication in the pathogenesis of autoimmune diseases has been the topic of much recent scholarship. Here I attempt to elucidate the molecular mechanism of vitamin D-mediated inhibition of the differentiation of CD4+ T cells into pro-inflammatory Th17 cells in MRL/lpr lupus prone mice by investigating how miR-125a expression is affected by dietary modulation of cholecalciferol (vitamin D3). MRL/MpJ and MRL/lpr mice were split into three experimental groups and fed specially formulated diets that varied in their concentrations of vitamin D. Plasma samples were tested for their concentrations of vitamin D, IL-6, and IL-17 by enzyme linked immunosorbent assay (ELISA). Additionally, Th17 cells in the mouse spleens were quantified via fluorescence activated cell sorting (FACS) analysis. Finally, miR-125a expression in spleens and inguinal lymph nodes was quantified using real time quantitative polymerase chain reaction (RTq-PCR). Ongoing studies, made possible by my work up and to this point, will contribute to our understanding of the mechanism by which vitamin D controls CD4+ T cell differentiation into Th17 cells and to our understanding of and ability to treat autoimmune and other chronic conditions such as systemic lupus erythematosus (SLE).
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Hilt, Miranda, "miR125a as Molecular Target of Vitamin D Mediated Inhibition of CD4+ T Cell Differentiation into Th17 cells in MRL/lpr Lupus-prone Mice" (2023). Undergraduate Distinction Papers. 105.