Document Type
Thesis
Abstract
Research in the Weidanz laboratory is focused on cellular molecules which inhibit immune activation, known as immune checkpoints. One example is HLA-E, which can modulate immune responses at homeostasis or in the context of cancer. HLA-E typically acts by presenting short canonical peptides (VL9s) and binding to CD94/NKG2A receptors on NK cells and T cells. The Weidanz laboratory’s research has found that in the absence of these VL9 peptides, HLA-E binds to another immune checkpoint, VISTA, instead of CD94/NKG2A. Therefore, the HLA-E/VISTA interaction is peptide-dependent. The current study aims to determine if this peptide-dependent interaction is evolutionarily conserved using the homologous proteins from other species. Specifically, it investigates the interaction between Qa-1b, the murine equivalent of HLA-E, and VISTA. To evaluate this, MHC refolds, resonance sensor technology (ResoSens), ELISA, and Klickmer® v technology were employed to analyze peptide-dependent binding interactions. This research has implications for cancer immunotherapy and future clinical studies.
Disciplines
Medical Immunology
Publication Date
12-1-2024
Language
English
Faculty Mentor of Honors Project
Jon Weidanz
License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Recommended Citation
Glenn, Julia, "DETERMINING EVOLUTIONARY CONSERVATION OF MHC-E AND VISTA INTERACTION" (2024). 2024 Fall Honors Capstone Projects. 22.
https://mavmatrix.uta.edu/honors_fall2024/22