Making the body forget psoriasis

Psoriasis is considered one of the common chronic diseases in Sweden and is likely found in more than 600,000 people. It is a chronic inflammatory disease in which the immune system’s T cells – whose job is to recognise harmful substances and invaders such as viruses and bacteria – become overactive and release signalling substances that cause skin cells to grow faster than normal. At the same time, Treg cells, the immune system’s regulators, function poorly and are unable to slow the immune response as they should. This leads to red, scaly and inflamed skin.

Searching for trigger factors


Albert Duvetorp is a senior consultant in dermatology and a researcher at Lund University and Skåne University Hospital. He studies trigger factors for psoriasis, and one ongoing study concerns the Koebner phenomenon, meaning that new lesions appear on skin that has been damaged, for example by cuts, scratch marks or burns. About 40 per cent of all patients say they have developed psoriasis in connection with skin injury, and Albert Duvetorp therefore wanted to investigate which proteins are formed in the skin.

Because psoriasis often varies over time, biomarkers could make it possible to start treatment just before a patient experiences a flare-up

 
“Our goal is to find a protein pattern for psoriasis that can provide clues about how the disease is activated by different triggers such as infection, season or stress. If we can identify biomarkers, that knowledge could be used to tailor treatment. Because psoriasis often varies over time, biomarkers could make it possible to start treatment just before a patient experiences a flare-up.”
 
Psoriasis patches often return to the same place on the skin where the disease has appeared before. There is an immunological memory in the T cells, and surrounding cells tend to fall back into old, well-worn “genetic paths.” Modern psoriasis treatment therefore suppresses the T cells, which reduces the number of memory T cells and helps the body restore epigenetic changes*. Patients who have not had the disease for long and who respond quickly to these medications in particular seem to reset the body’s psoriasis memory to a greater extent.

Obesity makes it worse


Research is now under way on how best to achieve this super-response. People who are overweight often have more troublesome psoriasis. Fat tissue increases inflammation, makes the lesions more severe and reduces the effect of treatment. Obesity also means a higher risk of cardiovascular disease, fatty liver disease, diabetes and metabolic syndrome – conditions that often occur alongside psoriasis.
 
“There are several studies on diet showing that patients with severe psoriasis generally have poorer dietary habits than those with the milder form. But by changing your lifestyle, you can partly influence your disease.”
 
Today, effective treatments are available for moderate to severe psoriasis. Biological injectable drugs, which inhibit the signalling substances of T cells, are still both affordable and effective. But the newest psoriasis research is not only about blocking inflammatory signalling substances; it is also about understanding how the immune system’s braking mechanisms – including Treg cells – work and why they fail in this disease.
 
“Studies are also being carried out on how weight-loss drugs together with inhibitors of signalling substances may affect the disease, since obesity has been so central to the development of psoriasis,” concludes Albert Duvetorp.
 
*Epigenetic changes control which genes are active (switched on) or inactive (switched off) without altering the DNA sequence itself. They act like switches influenced by environment and lifestyle, such as diet, smoking and stress.
 
Text and photo: Åsa Hansdotter
The article was previously published in the journal Vetenskap & Hälsa, 2026.