NPF psoriasis researcher puts the “auto” in autoimmune disease

| Melissa Leavitt

You might think of psoriasis as a case of mistaken identity.

Your immune system decides that something in your body is actually a foreign invader, and pounces on it with an inflammatory response. But what exactly is that substance that your body mistakes for something dangerous?

New research funded by the National Psoriasis Foundation has identified the culprit that may set that misguided immune response into motion. According to the findings, an antimicrobial peptide known as LL37 could trigger psoriasis in people predisposed to the disease. 

Think of antimicrobial peptides as the body’s own antibiotics. LL37 plays a key role in protecting injured skin, providing an important defense against harmful bacteria, the researchers explain. But in some people with psoriasis, LL37 actually serves as an autoantigen. In other words, your body thinks LL37 is the enemy, such as a disease-causing bacteria or virus. When your body attacks it, it is actually attacking itself.

Although scientists have long recognized psoriasis as an autoimmune disease, the autoantigens that trigger the disease have been poorly understood, the researchers note. This study, published last week in the journal Nature Communications and funded through a 2011 Translational Grant to a co-author of the paper, Dr. Antonio Costanzo, is the first to identify LL37 as a possible autoantigen in psoriasis.

Prior to this study, researchers already knew that LL37 was an important player in psoriasis, Costanzo said. LL37 is overexpressed in psoriatic skin, and is involved in the activation of a kind of immune cell known as dendritic cells, he explained.

But after examining blood and skin samples from a group of people with psoriasis, researchers discovered that LL37 doesn’t just enhance immune activity. It may get the inflammatory ball rolling.

According to the findings, LL37 triggers an immune cell response in 46 percent of people with psoriasis—and up to 75 percent of people with moderate-to-severe disease. The type of immune cells triggered by LL37 produce key cytokines, or pro-inflammatory proteins, involved in psoriasis, such as interleukin-17, the researchers report.

Understanding the role of LL37 may also help explain how people who are genetically predisposed to psoriasis develop the disease. Researchers found a connection between the immune cell response to LL37 and certain genes that put someone at risk for psoriasis. This finding could shed new light on how these susceptibility genes function to trigger psoriasis, according to Costanzo.

The research team is currently working on new ways to inhibit LL37, which could provide new treatment options for people with psoriasis, Costanzo said.


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