Author ORCID Identifier
0009-0001-6874-3498
Month/Year of Graduation
12-2024
Degree Name
Bachelor of Science (B.S.)
Department
Biology
First Advisor
Paul W. Denton
Abstract
In the Denton Immunobiology Laboratory, we observed an unexpected circumstance when human peripheral blood mononuclear cells (PBMCs) were exposed to an immunotherapy drug, a toll-like receptor 9 (TLR9) agonist, leading to reduced surface CD16a levels on a specific subset of PBMCs, human natural killer (NK) cells [4]. To kill pathogenic cells, NK cells have two distinct killing methods: direct killing – not the subject of this proposal – and antibody- dependent cell-mediated cytotoxicity (ADCC). ADCC requires antibodies to help the NK cells recognize diseased cells and both ends of the antibody must be engaged. The antigen binding fragment (Fab) binds to a molecule on the pathogenic cell while the other end, the constant fragment (Fc), binds to an Fc receptor. Human CD16a, a Fc𝛾III receptor, is a binding site for the Fc of IgG antibodies (which are used in our experiment). The series of bindings is critical for human NK cell-mediated ADCC. Due to the reduction of CD16a levels on the human NK cells, the immunotherapy did not boost NK cell-mediated ADCC as suggested by other researchers in prior publications [9, 10, 15, 16, 17, 20]. This thesis project will study the changes in surface CD16a levels on NK cells over time after the introduction of TLR9 agonism. Other specific findings are not in the abstract since they are redacted from the paper due to material transfer agreement requirements.
Recommended Citation
Truong, Angela N., "Longitudinal Kinetics of Surface CD16 on Human Natural Killer Cells when Peripheral Blood Mononuclear Cell Pools are Treated with a Toll-like Receptor 9 Agonist" (2024). Theses/Capstones/Creative Projects. 334.
https://digitalcommons.unomaha.edu/university_honors_program/334