Three proteins cause inflammation in psoriasis

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[size=34]Psoriasis[/size]
In a basic research study, with cell lines and laboratory animals, immunologists from La Jolla, California, conclude that there are three proteins that, when interacting with each other, trigger the inflammatory process that gives rise to psoriasis. In this disease, as explained by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, in the United States, the immune system works too hard, causing certain areas of the skin to become scaly and inflamed. Psoriasis usually affects the scalp, elbows, and knees.
Sometimes psoriasis symptoms are cyclical, with flare-ups lasting a few weeks to several months, followed by times when there is improvement (that is, they go into remission). Psoriasis patients may be at higher risk for other serious conditions, including psoriatic arthritis, heart attacks or strokes, low self-esteem, anxiety, and depression.
In a work that appeared seven years ago in Actas Sifiliográfica, a publication of the Spanish Academy of Dermatology, specialists from the Autonomous University of Barcelona (UAB) and the Germans Trias i Pujol hospital concluded that the estimated prevalence of this disease in Spain was 2 , 3%, without statistically significant differences between sexes.
The prevalence in the different age groups followed an upward curve until 60-69 years. The highest prevalence corresponded to the central zone of the country with a cold and dry climate, although without significant differences with other regions. Its conclusions state that “the prevalence of psoriasis in Spain is significantly higher than that estimated in previous studies. This increase could reflect a better knowledge and diagnosis of the disease rather than a real increase in prevalence ”. In another study published fifteen years earlier, the prevalence of psoriasis in Spain was 1.4%.
In the last decade, the appearance of biological agents has revolutionized the treatment of psoriasis, increasing the prospects for efficacy and safety with respect to previous therapies.
The proliferation and establishment of these new therapeutic possibilities, consistent with the pathogenic knowledge of the disease – say the UAB experts – has been reflected in an exponential growth of both the scientific literature and the general press regarding the disease. psoriasis, facilitating an increase in the reasons for consultation for this cause, easier recognition of the disease in primary care and also better access to experts in this disease.

Potential treatment for psoriasis

Although there are effective treatments for psoriasis, not all patients respond equally to these therapies, and for many, relief is temporary. As Professor Michael Croft of the La Jolla Institute of Immunology and lead author of this study that appears in Science Immunology now points out, “These therapies do not reduce disease by 100% and they do not cure it. And if these drugs are withdrawn from patients, the disease almost always returns.
Now Professor Croft and his team at the La Jolla Center for Autoimmunity and Inflammation have discovered how a key protein called TWEAK damages skin cells in psoriasis patients. Their findings, in mice and with human skin cells, suggest that TWEAK may help control the disease. “We believe that this protein could be considered a potential target for the treatment of psoriasis,” says Rinkesh Gupta, a member of this team of immunologists.
The findings build on previous work from Professor Croft’s Laboratory, which shows that TWEAK can interact with the most common type of skin cell, called a keratinocyte. When investigating TWEAK-deficient mice, the researchers found that it is an inflammation factor in a psoriasis model. The new study shows that this protein does not work alone. By studying human keratinocytes, they discovered that it binds to two other proteins, called tumor necrosis factor (TNF) and interleukin-17 (IL-17), to trigger inflammation.

TWEAK inhibitors as human therapies

This trio appears to control the production of inflammatory molecules and the expression of additional proteins associated with inflammation in patients with psoriasis. “The fact that they act together suggests that the disease is essentially driven by all three particular proteins at the same time,” emphasizes Professor Croft. “The main implication is that TWEAK will also be a good drug target, as has already been shown for TNF and IL-17,” he says.
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