Graduation Year

2026

Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts

Department

The Department of Natural Sciences

Second Department

Biochemistry

Reader 1

Jeniffer Hernandez

Reader 2

Bethany Caulkins

Abstract

CD4+ helper T cells are specialized members of the immune system, allowing for the activation of the adaptive immune system through secretory signals and antigen presentation. Overactivation of CD4+ T cells can lead to increased autoimmune responses, which afflict 4% of the world’s population. Th17 cells provide defenses against extracellular pathogens, but are also key influences within autoimmune responses, causing inflammation of tissues. G-protein coupled receptors (GPCRs), which are found on CD4+ T cells, participate in over 30% of approved drug treatments. GPR65 is a critical regulator of Th17 cell pathogenicity, and GPR65 knockout in a mouse model reduced its susceptibility to multiple sclerosis. Drug treatments targeting human Th17 cells have been shown to modulate the production of interleukin-10, an anti-inflammatory cytokine that promotes Th17 cell pathogenicity. To better characterize the role of GPR65 within human T cells, Jurkat immortalized human T lymphocyte cells underwent a cotransfection for a knockdown of GPR65. This knockdown was confirmed through Fluorescence-Activated Cell Sorting (FACS) and a western blot. Relative qualitative PCR supports the suppression of cytokines within the knockdown cells that are associated with the differentiation of Th17 cells. Future studies will characterize the modulation of cellular respiration in the GPR65KD cells and confirming RNA-sequencing within the cell.

Download

This thesis is restricted to the Claremont Colleges current faculty, students, and staff.

Share

COinS