Sophia Schneider
Pronouns: She/her
Research Mentor(s): Jintao Xu
Research Mentor School/College/Department: Internal Medicine / Medicine
Program:
Authors: Sophia Schneider, Jintao Xu, Kristie Goughenour, Rylan Hissong, Michal Olszewski
Session: Session 4: 1:40 pm – 2:30 pm
Poster: 35
Abstract
Cryptococcus neoformans is a fungal pathogen found throughout the environment that infects people through the lungs and spreads to the brain. It can have life-threatening effects, particularly to those who are immunocompromised. A major part of the immune response, type 1 conventional dendritic cells (cDC1) cells are crucial in Th1 polarization, which is necessary to control fungal infections; however, we have observed that C. neoformans infection impairs the activation and functionality of cDC1 in pulmonary context. In order to offer specific targets to enhance host immune defense and inform potential immunotherapies and vaccines, our research explores cDC1 and its effects. To elucidate the mechanisms behind cDC1 inhibition during pulmonary C. neoformans infection, a comparative analyses of two models: a protective model and and a non-protective model, where the non-protective model resulted in decreased IFN-? production by cD4+ T-cells at 14 days post infection. Through the analyses, we were able to glean that lowered IFN-? production is correlated with diminished cDC1 activation. Additionally, we were able to observe that the non-protective model displayed an upregulation of type-1 IFN pathway genes in comparison with the protective model. Future studies are needed to test if the type-1 IFN pathway plays a role in limiting cDC1 activation and subsequent anti-cryptococcal immune responses in the host. Our study may reveal novel regulatory mechanisms of cDC1 inhibition and targets for boosting host immunity against C. neoformans.
