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Dr Lucille Rankin – Immunology division

09/04/2025 1:00 pm - 09/04/2025 2:00 pm
Location
Davis Auditorium

WEHI Wednesday Seminar hosted by Professor Daniel Gray
 

Dr Lucille Rankin

Senior Research Officer – Gray Laboratory, Immunology division, WEHI

 

Context and Tissue Specific Control of FoxP3+ Treg Diversity

 

Davis Auditorium

Join via SLIDO enter code #WEHIWednesday

Including Q&A session
 

 

 

Tissue-resident immune cells have emerged as an integral part of tissue homeostasis. Beyond their function in defending against pathogens, these cells have a remarkable ability to rapidly adapt to constantly changing environments and regulate local tissue health. These functions are particularly evident in the gastrointestinal tract, where it is crucial that a peaceful co-existence between host and commensal microbes/dietary antigens are maintained.

 

FoxP3+ regulatory T cells (Tregs) are a specialized immunosupressive population of CD4+ T cells that are highly abundant in the gut, and preserve this delicate relationship between the host, diet and microbiota. When this balance is disrupted and Tregs are lost, colitis, microbial disbiosis and chronic inflammatory diseases can arise. A feature of gut-resident Tregs is that they are highly heterogenous, being characterised by their expression of key transcriptions factors: Gata3 drives a distinct program in thymic-derived Tregs, while RORγt is a key regulator of microbially-induced Tregs. Each of these subsets respond to discrete environmental cues, however, the complex factors driving their location, survival and functions in the gut remains to be fully understood.

 

In this seminar, Dr Rankin will explore two potent pathways that specifically modulate gut-resident Treg diversity: 1) through an acute dietary intervention – dietary tryptophan depletion, and 2) through the manipulation of the programmed cell death pathway necroptosis.  This research opens new therapeutic avenues to modulate tissue resident Treg subsets for correcting gastrointestinal and metabolic disease.

 

All welcome!

 

 

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