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

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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