Graduation Year

2024

Date of Submission

12-2023

Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts

Department

Neuroscience

Reader 1

Dr. Marlys S. Fassett

Reader 2

Dr. Tessa Solomon-Lane

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Terms of Use for work posted in Scholarship@Claremont.

Rights Information

2024 Matthew Na

Abstract

Nervous system and immune system communications have been widely researched in recent years. One of the many ways in which the nervous system communicates with the immune system is via small chains of amino acids that serve as chemical messengers known as neuropeptides. Unlike neurotransmitters, which primarily facilitate communication between cells of the nervous system, neuropeptides communicate with cells outside the nervous system, such as vascular endothelial cells or hematopoietic cells. Recent research has looked into how the nervous system, via neuropeptides, communicates with CD4 lymphocytes, also known as CD4 T cells, which are known to be one of the key drivers of the immune response including that of the skin. My research mentor at UCSF recently discovered that CGRP signaling inhibits basic functions of CD4 T cells during an allergic immune response. Because sensory neurons have been shown to influence psoriasis-like skin inflammation, I hypothesized that CGRP could also impact differentiation of CD4 T cells in the setting of Th17 (psoriasis-type) cellular differentiation. We found that Th17 cells express both subunits of the CGRP receptor. We also found that CGRP reduces Th17 cell differentiation in vitro, as measured by IL-17A cytokine production. Analogous experiments performed using T cells from Ramp1 knockout mice resulted in no changes in cytokine production between CGRP present and CGRP absent groups, confirming that CGRP signaling requires RAMP1 in this. These findings indicate that CGRP, through the RAMP1/CLR heterodimer, mediates inflammatory responses via suppression of Th17 cells and its primary cytokine IL-17A.

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