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Hannah Brown, PhD




Research Fellow




Postdoctoral Research Fellow




Hannah E. Brown*, Nida S. Khan, Geneva N. Kwaku, Jenny Tam, Daniel Z. Miranda, Josh D. Nosanchuk, Jatin M. Vyas

Candida albicans extracellular vesicles trigger type I IFN signaling via cGAS and STING

After experiencing systemic sexism in the scientific field and witnessing the drop-off of women after graduate-level training, I feel passionate about increasing female visibility in academia especially through participation in events like this symposium. My eventual goal is to become a professor with a research lab of my own. I need to converse with other strong female scientists and researchers at this institution so that I can build a strong mentor team to help me reach these goals and this symposium is the perfect opportunity to do so. Thank you in advance for your consideration.


Fungal infections are pathogens pose an increasingly relevant threat, despite availability of cytotoxic antifungals. The innate immune system is the first line of host. A major output of innate immune response, the first line of host defense against invading fungi, including, is production of Type I interferons (IFNs), which has been linked to human Candida albicans (Ca) infections. We aim to understand how the STING pathway, an IFN-producing and DNA-sensing pathway, is involved in host responses to Ca. We demonstrated that mice lacking STING pathway elements are resistant to Ca infection.


The extent to which DNA-carrying extracellular vesicles (EVs) from Ca induces the STING pathway was identified by Western blotting and ELISA. Nanostring technology was utilized to uncover transcriptional responses to pathway activating. Finally, I examine functional consequences of activation with phagocytosis, fungal burden, and inflammation assays.


Ca EVs induced expression of Viperin, an IFN-stimulated gene and known STING pathway output, in macrophages. This induction was cGAS- and STING-dependent. Nanostring analysis identified that 70% of known ISGs are turned on in a cGAS- and STING- dependent manner in response to EVs. Finally, we demonstrated that anti-inflammatory steroid treatment in macrophages dampens STING activation.


Overall, these studies reveal a novel mechanism of STING-pathway activation and provides better understanding of early, innate immune response to a clinically significant fungal pathogen.