Researchers develop 3D printed human skin models to better investigate immune responses
New technology from Queen Mary University of London enables lab-based investigation of human immune dysfunction and inflammatory disease without using traditional cell culture methods or animal models.
Scientists at Queen Mary University of London have developed advanced 3D printed human skin models that mimic key immune responses in real human tissue, opening the door to more accurate studies of skin diseases and inflammatory processes.
Developed by researchers at the Blizard Institute, the novel models include blood vessel-like microfluidic channels that can deliver circulating immune cells into the system, allowing scientists to study how the immune system reacts to threats such as bacteria without needing to rely on animal models.
The paper was published in Advanced Science. The studies were carried out by Dr Sarah Hindle as part of her PhD, along with Holly Bachas Brook and Dr Alexander Chrysanthou in Prof. John Connelly’s group. The work also involved collaboration with Dr Matthew Caley in the Centre for Cell Biology and Cutaneous Research and Dr Emma Chambers in the Immunobiology group.
Human skin is the body’s first line of defence against external threats like bacteria, allergens and environmental toxins. Studying its immune responses in a lab setting has long been a challenge, due to the complexity of interactions between different skin cells, blood vessels and immune cells.
The new technology uses 3D printing to build human skin models with embedded microfluidic channels that simulate the behaviour of blood vessels. This enables the delivery of immune cells into the system, closely replicating how the body would respond to inflammation in real human skin.
The research shows that the model replicates key aspects of acute inflammatory responses, including the recruitment and differentiation of immune cells in response to purified bacterial products, demonstrating a significant step forward in studying human-specific immune responses under controlled lab conditions.
The team also used a cutting-edge technique called single-cell transcriptomic profiling, an approach that measures gene activity in individual cells, to confirm the model’s accuracy at a molecular level.
One of the study’s most surprising findings was how different cell types in the skin reacted uniquely to the same inflammatory trigger. Keratinocytes – cells in the outermost skin layer – responded rapidly but then began to shut down their response, while fibroblasts – found in the deeper dermis – activated more slowly. This led to two distinct waves of immune cell recruitment, a phenomenon the researchers plan to explore further to uncover the molecular pathways involved.
The new skin models could have further applications, such as testing the safety and effectiveness of new drugs, leading to better treatments for patients with skin conditions such as eczema, psoriasis, and age-related inflammation.
The use of human-based lab models like these also aligns with the growing push to reduce reliance on animal testing in medical research.
Looking ahead, the team believes their platform could be adapted to model immune responses in other barrier tissues, such as the lungs or gut, offering a powerful tool to explore immune function across the human body.