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New Study Shows Psoriasis DNA Hotspots

Posted: February 10, 2009

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The team also found that genetic signals for proteins activated by TNF- a key signaling molecule involved in inflammation, are distinct from the patterns—TNFAIP3 and TNIP1—show strong in healthy controls. Two genes activated by TNF- association with psoriasis. Together, these genes limit immune responses. Genetic alterations in this "brake" may allow the immune system to work overtime within the skin. Variants of TNFAIP3 also have been associated with rheumatoid arthritis and lupus, two other autoimmune conditions.

The fourth novel hotspot implicates two "next-door neighbor" genes, IL4 and IL13. These genes support development of Th2 cells, a type of immune system T cell. Any condition that leads to too few or too many Th2 cells in relation to other types of T cells may result in disease, including psoriasis.

This new research, together with recent immunology work by Elder and colleagues, links four psoriasis loci (IL12B, IL23A, IL23R and IL4/IL13) together in a common functional pathway.

Implications

The large library of genetic data increases the number of proteins and pathways that can be targeted by emerging therapies to fight psoriasis. Once the full catalog of psoriasis genes has been identified, it may be possible to generate a "psoriasis gene profile" that can accurately predict one's risk of developing the disease. Such work may one day help assess risk of heart attack and stroke, because psoriasis carries an increased risk of coronary artery disease, and TNFAIP3 has also been shown to influence risk of coronary artery disease in mice.