Psoriasis – Viral Infection, Interleukin-29, Th17, Antiviral Proteins

Last year the researchers from Germany published their discovery that atopic dermatitis (atopic eczema) sufferers have lower levels of antiviral proteins in their skin when compared to psoriatics. This is an interesting fact in my opinion since currently I consider psoriasis as a disease involving the viral infection.

Here is an excerpt from their press release:

An immune messenger determines

How the skin of patients with psoriasis protects itself from virus infections

Psoriasis and atopic dermatitis are the two most common chronic diseases of the skin, from which over 40 million people suffer in the US and in EU alone. They cause persistent visible changes of the skin that severely impact the quality of life of the patients. In addition, the damaged skin barrier enables pathogens, such as viruses, to penetrate the skin and multiply. Surprisingly, only atopic dermatitis patients show a high incidence of cutaneous viral infections, which exacerbate the course of atopic dermatitis and if not treated promptly, might be life-threatening. The authors of the just-published study show that compared to the skin of patients with psoriasis, the skin of atopic dermatitis patients produces smaller quantities of what are known as antiviral proteins, which inhibit viral replication. In the search for the trigger responsible for these differences in protein production in the two skin diseases, the research team came upon the immune messenger interleukin-29.

As the subtitle in the press release says: “How the skin of patients with psoriasis protects itself from virus infections”

When we think about this a little we have to ask the question: Psoriasis is a defect in the immune system, but that defect cause that the skin is protected better from viral infections?

Of course that it is possible but that sounds somehow weird. If we would consider psoriasis as autoimmune disorder then there is no reason for the body to make the extra protection from the viruses. But if we would consider psoriasis as viral infection (what I do consider) then it makes sense for the body to make the extra antiviral proteins in the skin to slow down the viral replication.

“Of the thirty messengers produced by the immune cells that we examined in psoriatic skin, we only found a correlation with the quantities of antiviral proteins for interleukin-29,” explains Dr. Kerstin Wolk from the Institute of Medical Immunology at the Charité, one of the study’s two first authors. “In fact, interleukin-29 is present in psoriatic skin, but not in affected skin of atopic dermatitis patients.” Removing this immune protein from skin samples taken from patients with psoriasis diminishes the quantity of antiviral proteins in these samples. Using experiments with healthy skin, skin models and isolated cells from the upper layer of the skin, the team additionally showed that interleukin-29 is able to stimulate the production of antiviral proteins, and thereby to protect the skin cells from viral infection.

Moreover, the researchers showed that interleukin-29 is produced by a specific population of immune cells known as Th17 cells. “These cells promote the production of antiviral proteins and thus, anti-viral defences in the skin cells,” explains Dr. Katrin Witte from the Institute of Medical Immunology at the Charité, also a first author of the study. Thus, they simultaneously uncovered a new function of the immune system.

Science Translational Medicine, 25 September 2013, Vol. 5, Issue 204, p. 204ra129, Sci. Transl. Med. doi: 10.1126/scitranslmed.3006245

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