Scientists have uncovered why only some people with psoriasis go on to develop painful joint inflammation.
Between 20 and 30 percent of people with psoriasis eventually develop a second, more disabling problem: painful joint inflammation. Known as psoriatic arthritis, it can quietly worsen and, without treatment, leave permanent damage in bones and joints.
Researchers have long struggled to explain why only certain patients make this shift from skin symptoms to joint disease. Now, a group at the Department of Medicine 3 – Rheumatology and Immunology at Uniklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), reports that they have pinpointed the immune cells that leave inflamed skin, reach the joints, and set the stage for inflammation.
Their results, published in Nature Immunology, point toward strategies that could help block psoriatic arthritis before it becomes established.
How inflammatory cells travel from the skin to the joints
The team found that psoriasis drives the formation of specialized immune precursor cells in affected skin. “These cells can migrate from the skin to the bloodstream and from there to the joints,” explains Dr. Simon Rauber, head of the working group at the Department of Medicine. “It is interesting that the mere migration of immune cells into the joint is not sufficient to trigger inflammation there.”
How inflammatory cells infiltrate the joint
To understand what turns a visit into a flare, the researchers looked at the joint environment itself. Once the traveling immune cells arrive, they run into fibroblasts, connective tissue cells that help maintain and defend joint tissue, and they do not respond kindly to these unexpected newcomers.
“The protective function of these connective tissue cells is usually considerably reduced in people who develop psoriatic arthritis,” says Prof. Dr. Andreas Ramming, team leader and deputy head of department at Department of Medicine 3. “As a result, the inflammatory cells that enter the joint cannot be brought into check, and go on to trigger an inflammatory reaction in the joint.” The results provide an explanation for why some psoriasis patients go on to develop joint disease as well.
Early detection and prevention before the disease affects the joints
As the migratory immune cells can already be detected in the blood before triggering inflammation in the joints, this could act as an early warning signal in the future, allowing patients at risk to be identified in time. In the future, treatment strategies could be aimed specifically at intercepting these inflammatory cells and preventing them from triggering inflammation in the joints.
Reference: “Skin-derived myeloid precursors and joint-resident fibroblasts spread psoriatic disease from skin to joints” by Maria G. Raimondo, Hashem Mohammadian, Mario R. Angeli, Stefano Alivernini, Vladyslav Fedorchenko, Kaiyue Huang, Richard Demmler, Peter Rhein, Cong Xu, Yi-Nan Li, Raphael Micheroli, Zoltán Winter, Aleix Rius Rigau, Charles G. Anchang, Alina Soare, Markus Luber, Hannah Labinsky, Jiyang Chang, Claudia Günther, Ursula Fearon, Douglas J. Veale, Francesco Ciccia, Jürgen Rech, Michael Sticherling, Tobias Bäuerle, Jörg H. W. Distler, Mariola S. Kurowska-Stolarska, Matthias Mack, Arif B. Ekici, Adam P. Croft, Oliver Distler, Hans M. Maric, Caroline Ospelt, Juan D. Cañete, Maria A. D’Agostino, Georg Schett, Simon Rauber and Andreas Ramming, 2 January 2026, Nature Immunology.
DOI: 10.1038/s41590-025-02351-z
The research is being funded by the German Research Foundation (DFG) within the framework of the CRC/TRR 369 – “DIONE: Degeneration of bone due to inflammation,” by the European Research Council (ERC) as part of the project “Barrier Break,” and by the Interdisciplinary Center for Clinical Research in Erlangen (IZKF) as part of the project “Tissue imprinting of skin-derived immune cells in psoriatic arthritis.”
Never miss a breakthrough: Join the SciTechDaily newsletter.
Follow us on Google and Google News.