Psoriasis causes your body to make new skin cells too quickly. These cells tend to pile up and form spots, bumps, and thick scaly patches called plaques that can be uncomfortable.
Scientists think psoriasis happens when your immune system starts to attack your body without obvious reason.
Your immune system uses tiny proteins called cytokines to communicate between cells. These proteins are an important part of why certain cells grow more and others grow less. Some cytokines appear to play a key role in psoriasis.
What Do Your Genes Have to Do With It?
Genes are sets of plans inside every cell in your body. They tell your hair to grow brown or blonde, your eyes to be green or blue, your feet to grow narrow or wide, and a million other details.
Faulty genes can also sometimes cause things to go wrong. Your heart might grow in the wrong way, or the faulty genes might put you at a higher risk for diseases like cancer, Parkinson’s, or psoriasis.
Scientists know that your genes play a part in psoriasis because you’re more likely to get it if blood relatives also have it.
And because scientists know that certain cytokines affect psoriasis, they have focused on the genes that help make those cytokines.
Certain variations, or “mutations,” in these genes make you more likely to get psoriasis. (A gene mutation is a change in the way a gene normally works). But it’s important to note that there is no gene – or gene mutation – that guarantees you will get psoriasis. Nor does a lack of certain genes or mutations mean you won’t get psoriasis.
Which Cytokines Make a Difference in Psoriasis?
The roots of psoriasis are complex and scientists don’t yet understand all of the factors or how they fit together. They do know that there are both genetic and environmental factors that contribute to the disease. Also, scientists have learned enough about the higher levels of certain cytokines in certain people with psoriasis to make medicines that help symptoms in many people.
For example, people with inflammatory diseases like psoriasis tend to have higher levels of certain proinflammatory cytokines. These include:
- TNF-alpha
- IL-23
- IL-17 (especially IL-17A and IL-17F)
Scientists continue to study which cytokines affect psoriasis and which gene mutations might be to blame.
Which Treatments Specifically Target Cytokines?
Scientists have developed a number of “biologic” medicines that improve symptoms of psoriasis by neutralizing certain cytokines. Biologic medicines work by targeting certain specific parts of your immune response.
A unique group of medicines that target the IL-17 group of cytokines or their receptors includes:
Other biologics work to slow or stop body processes that cause joint damage. These meds target TNF-alpha. These medications include:
- Adalimumab (Humira)
- Certolizumab pegol (Cimzia)
- Etanercept (Enbrel)
- Infliximab (Remicade)
What’s Ethnic Background Got to Do With It?
Quite a bit, it seems. Different ethnic groups have different genetic trends. This can be something as obvious as skin color and eye shape, but it can also express itself in certain diseases. Or it can get as specific as the way cytokines are likely to mutate in different populations.
For example, a very particular cytokine-linked genetic variation is more likely to develop in Korean people. Scientists know that this group of Koreans with psoriasis tends to respond well to treatment with the biologic drug infliximab. On the other hand, Spanish or Japanese people don’t seem to have this particular genetic variation.
A different pair of mutations was found in the Spanish population. One of the variations (rs79877597) is linked to more serious types of psoriasis and psoriatic arthritis. In white people, one genetic mutation (rs4819554) suggests a better response to certain medications that target TNF-alpha.
There has been exciting progress in recent years in the treatment of psoriasis. Scientists will continue to research how different genetic, ethnic, and environmental factors interact to cause the disease.