Our Science

 
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M. tuberculosis (Mtb)

We love Mycobacterium tuberculosis! Well, no — we actually hate it, but we are obsessed with it. It causes TB and kills ~1.5 million people every year worldwide, making it [one of] the biggest infectious disease killers. There are antibiotics for TB, but you have to take them for months, and the side effects can be serious. Plus, with increasing antibiotic resistance, the first-choice antibiotics don’t always work anymore (and the second-choice antibiotics have even worse side effects and may not even work).

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Macrophages

Macrophages are very cool. They do amazing things, like eating everything around them and then figuring out if what they ate is a harmful pathogen or just a random piece of garbage. They’re really good at killing pathogens that constantly try to attack our bodies, but weirdly, they aren’t very good at killing Mtb. And that’s a problem for our bodies. We want to better understand why macrophages are so bad at killing Mtb so that we can figure out how to help them do better with new drugs.

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Host-pathogen interactions

We are obsessed with the arms race between Mtb and macrophages. The sneaky ways a macrophage senses Mtb and tries to respond. The maniacal ways Mtb evades detection and escapes destruction. It’s all very interesting biology, but really, we hope that understanding these things will help us contribute to finding better treatments for TB.

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Danger sensors

How does a macrophage recognize intracellular Mtb? What molecules are detected, and what sensors detect them? What are the downstream pathways activated by these detection events, and how do they impact infection outcomes? How are these pathways regulated to mount a response that effectively controls Mtb infection?

 
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Mtb effectors

How does Mtb modulate macrophages? How does it use its effectors to alter host cell biology, and which effectors regulate critical innate immune responses? What pathways can effectors target, and what is the biochemistry and molecular biology underlying their functions? How do these effectors and their impact on macrophages influence infection outcomes?

 
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Phase separation

How does phase separation impact innate immune responses? What proteins phase separate during Mtb infection, and how does phase separation alter their functions? How is infection-induced phase separation regulated? Can Mtb promote or inhibit infection-induced phase separation?