CPC-M scientists Mareike Lehmann and Maja Funk receive a grant of the Deutsche Forschungsgemeinschaft (DFG) to investigate age-related epithelial-immune cell interactions in the lung
As we age, our lungs also age—but the precise reasons why they become more prone to serious diseases like Chronic Obstructive Pulmonary Disease (COPD) and Idiopathic Pulmonary Fibrosis (IPF) remain elusive. Now, a new research project led by Dr. Mareike Lehmann and Dr. Maja Funk at the Munich site of the German Center of Lung Research (CPC-M, Helmholtz Munich) aims to uncover one crucial piece of the puzzle: how aging affects communication between lung cells and immune cells.
The project, named ARCTIC (short for Age-related changes in Epithelial-T cell interaction impair lung regenerative capacity) has been awarded funding from the German Research Foundation (DFG) as part of the Priority Program “Heterotypic Cell-Cell Interactions in Epithelial Tissues (HetCCI).”
At the heart of ARCTIC lies a fundamental question: Why does the lung lose its ability to repair itself with age?
In younger individuals, specialized epithelial stem cells help maintain the lung’s structure and function. But as we grow older, these cells become less capable of regenerating damaged tissue. According to prior studies, they also undergo changes such as cellular aging, including senescence, and shifts in gene regulation—factors that are likely to contribute to disease vulnerability.
What’s new is the suspicion that aging immune cells—specifically T cells—may play a key role in this breakdown of lung maintenance. The team’s early findings suggest that these immune cells not only accumulate in unusual areas of the lung as we age, but also change in behavior, becoming more inflammatory and less effective.
“Epithelial and T cells don't operate in isolation. They constantly communicate, and these interactions may change drastically in aged lungs,” says Dr. Lehmann. “We want to understand how these direct cell-to-cell contacts are altered during aging—and how this might impair lung repair mechanisms.”
By mapping out how aging affects these cellular interactions, the researchers hope to reveal new targets for preventing or treating age-related lung diseases. With ARCTIC, Lehmann and Funk are venturing into a relatively unexplored field that connects immunology, regenerative biology, and aging research.
“This project will help us get closer to understanding why the aging lung becomes so vulnerable—and ultimately, how we might intervene,” adds Dr. Funk.
The findings could one day lead to therapies that not only slow the progression of devastating lung diseases but also preserve lung health in old age.