The new study was led by Dr Vanessa Bryant, Professor Phil Hodgkin and Dr Susanne Heinzel with clinical expertise from Snow Centre Director, Professor Jason Tye-Din.

The research examined a type of immune cell known as CD4 helper T cells, which coordinate immune responses, fight infection and support antibody production.

“Our assay is a bit like winding up a toy and letting it go to see how long it runs and what tricks it performs.

“Our method reveals how well T cells read and store their activation signals to maintain their ‘momentum’ once the original stimulus is gone. and whether people with autoimmune disease have built-in differences in how their cells function.”

To explore this, researchers used centre’s pioneering Cyton2 Cell Timer model, which tracks immune cell activity over time.

The aim was to track the T‑cell “momentum”. Rather than continuously stimulating cells, as most laboratory tests do, the team briefly activated them, then removed all signals to observe what happened next.

“This allowed us to see how cells behave once the initial push has stopped,” Dr Bryant said.

“It reveals properties that are harder to detect under constant stimulation.”

The team measured how cells divided, survived and produced key signalling molecules, building a detailed picture of early immune behaviour.

Dr Bryant said this approach is an entirely unique way to measure immune responses, giving researchers new insights into how they can go awry.

“Understanding these early defects could lead to better ways to predict risk, monitor disease, and eventually develop treatments that restore healthy immune balance, not just manage symptoms through a gluten‑free diet.”

Contrary to expectations, immune cells from people with coeliac disease were not simply overactive. Instead, they showed weaker responses.

The study found CD4 helper T cells from people with coeliac disease:

• produced less interleukin-2, a key immune signalling molecule
• entered cell division more slowly
• were less likely to survive

“These differences were subtle but remarkably consistent,” said Dr Bryant.

Notably, the same pattern appeared regardless of sex or whether individuals were newly diagnosed or managing the condition with a gluten-free diet.

“This tells us the effect isn’t simply driven by inflammation or diet,” said Dr Bryant. “It suggests an underlying difference that may be linked to genetic risk.”

Although the study focused on coeliac disease, the findings may have broader relevance.

Autoimmune diseases affect around five per cent of the population, and many share overlapping genetic risk factors.

“If autoimmune risk is partly built into how immune cells behave from the start, this could change how we think about early detection,” said Dr Bryant.

While this approach is a research tool rather than a clinical test, it opens the door to combining genetic information with functional immune measurements to better predict disease risk.

Professor Tye-Din said the study highlights the power of the Snow Centre’s Cyton ‘cell-timer’ model to uncover hidden patterns in immune function.

“This gives us a new way to understand immune behaviour in greater detail. My hope is that these fundamental insights will eventually translate into clinically useful tools to inform assessments of disease risk.”

Rather than focusing only on immune cells that directly damage tissues, the study highlights the importance of cells that regulate and sustain immune responses.

“Although these helper cells aren’t always the main focus in autoimmune research, they may hold important clues to why disease develops in some people and not others,” said Professor Tye‑Din.

The team is now investigating whether similar immune patterns exist in other autoimmune conditions, and how early in life these differences appear.

“Our long‑term goal is to understand autoimmune risk well enough that we can act earlier – potentially even before disease begins,” said Professor Tye-Din.

To learn more visit the Snow Centre for Immune Health.