Date of Award

Spring 2006

Document Type

Legacy Thesis

Degree Name

Bachelor of Science (BS)




College of Science

First Advisor

Karen Aguirre


The immune system has evolved innate and adaptive responses to protect from invading microorganisms. Immune function is relatively well understood in the periphery, but qualitative differences exist when infection occurs in the central nervous system (CNS), and these differences are poorly understood. One cell activated in response to CNS infection is the brain-resident macrophage, or microglial cell. Microglia interact with T lymphocytes, which bind to the MHC class I-peptide combination. Past research has focused on microglia/CD8+ T cell interaction in viral models. However, the pathogenic fungus Cryptococcus neoformans, and other non-viral facultative and obligate intracellular pathogens represent a considerable portion of reported CNS infections. Such pathogens do not interfere with host cell gene expression as do viral pathogens, and therefore must be controlled by different mechanisms. This study focuses on the viability of CD8+ T cells after microglial activation in a non-viral system. As it is not known how CD8+ T cell homeostasis is maintained after CNS infection, the TUNEL assay was performed on activated microglial/ CD8+ T cell co-cultures after 48 and 120 hours in order to investigate if CD8+ T cell death is specifically a result of apoptosis (or programmed cell death). Positive results yielded for all conditions that the TUNEL assay was performed on. By using t-tests to statistically compare co-cultures with and without a super antigen added, it was found that a significant difference exists in apoptotic levels at a 48 hour time point that would not be found by simply random sample. This is biologically significant because it shows that there is crosstalk occurring between microglial cells and CD8+ T cells, and that apoptosis is the mechanism that CD8+ T cells undergo in vitro to establish homeostasis. Overall, understanding the detailed mechanism involved in CD8+ T cell antimicrobial function versus non-viral CNS pathogens is significant as it is a rational basis for designing immunotherapy or vaccines which elicit CD8+ T cell memory for hosts depleted of CD4+ T cells.