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Seminar | Poised to Die: Unique Sensitivity of GATA3⁺ Tissue Tregs to Necroptosis Shapes Barrier Function

28th October, 2026

2026OCT28_Lucille Rankin.jpg
Event Type:
Seminar
Venue:
IDRM, IMS-Tetsuya Nakamura Building, Seminar Rooms 1 & 2 OR online via Teams
Event Time:
15:30-16:30
Wheelchair Access:
Yes
Booking Requirement:
Registration is required for online attendees
Booking:
Book Online
Additional Details:

All University of Oxford members are welcome to attend this seminar.

About the speaker: 

Dr Lucille Rankin is a Senior Research Officer at WEHI in Melbourne, Australia whose research explores how environmental signals shape immunity and tolerance at barrier tissues, particularly the gastrointestinal tract. She completed her PhD with Professor Gabrielle Belz at WEHI, studying the development and function of innate lymphoid cells, before undertaking postdoctoral training in New York with Professor David Artis and Associate Professor Nicholas Arpaia. Her work has helped define how dietary, microbial and neuroimmune signals regulate tissue-resident immune populations. She now investigates how programmed cell death pathways interact with environmental signals to shape immune cell specialization, tissue homeostasis and repair.

Seminar Abstract:

Tissue-resident immune cells have emerged as critical regulators of tissue homeostasis. Beyond their role in host defense, they adapt to changing environmental cues to maintain local tissue function and promote repair.

Regulatory T cells (Tregs) are central to these processes, yet how specialized tissue-resident Treg subsets are selectively maintained remains poorly understood.

In this seminar, Dr Lucille Rankin will discuss a previously unrecognized mechanism controlling Treg subset dynamics. Her work demonstrates that tissue-reparative Gata3⁺ Tregs exhibit a unique intrinsic sensitivity to necroptosis, an inflammatory form of programmed cell death. Inhibition of Caspase-8 licenses this pathway, resulting in the selective depletion of Gata3⁺ Tregs and subsequent defects in tissue repair. 

These findings identify necroptosis as a therapeutically targetable critical regulator of tissue-adapted Treg states and reveal programmed cell death as an active mechanism shaping immune cell specialization within tissues.

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