Researchers, doctors, and scientists know a lot about what causes psoriasis. They know how to treat it, and they even know how to reduce your risk for future flare-ups. Still, there’s much more to discover.

As understanding about this common skin condition grows, scientists are producing smarter medicines and more effective treatments. In addition, researchers are trying to better understand why some people develop psoriasis and others don’t.

Keep reading to learn more about what’s on the horizon for psoriasis treatments and research.

Biologic medications are derived from natural sources, not chemical ones. They’re very potent. Biologics alter the way your immune system works by stopping it from sending out inflammation signals. This lowers your risk of symptoms.

Biologics are administered intravenously or via an injection.

Anti-interleukin-17 (IL-17) agents

Interleukin-17 (IL-17) is a cytokine, a type of immune protein. It induces inflammation. High levels of IL-17 have been found in psoriatic lesions.

Stopping the protein or reducing the level of it in your body may help clear psoriasis. Some medicines are designed to target the IL-17 receptor or the IL-17 itself. This helps to prevent an inflammatory reaction.

Some anti-IL-17 drugs that have been approved by the Food and Drug Administration (FDA) include:

  • secukinumab (Cosentyx)
  • ixekizumab (Taltz)
  • brodalumab (Siliq)

Another anti-IL-17 drug, bimekizumab, is currently undergoing phase III clinical trials.

IL-12/23 inhibitors

IL-12/23 inhibitors target a subunit that’s shared by the IL-12 and IL-23 cytokines. Both cytokines are involved in inflammation pathways associated with psoriasis.

Ustekinumab (Stelara) is an IL-12/23 inhibitor that’s FDA-approved to treat psoriasis.

IL-23 inhibitors

IL-23 inhibitors target a specific subunit of IL-23. These inhibitors can then effectively block the protein from carrying out its function.

Some FDA-approved IL-23 inhibitors are:

  • guselkumab (Tremfya)
  • tildrakizumab (Ilumya)
  • risankizumab (Skyrizi)

JAK inhibitors

JAK proteins are located within cells and are associated with receptors on the cell surface. The binding of molecules — such as cytokines — to the receptor causes a change in the molecule’s shape. This activates the JAK proteins and initiates signaling pathways that can be involved in inflammation.

JAK inhibitors work to prevent JAK proteins from functioning properly. These drugs are available as oral agents, which is differ than other biologic drugs.

Tofacitinib (Xeljanz) is an example of a JAK inhibitor. While this drug is currently approved for the treatment of psoriatic arthritis (PsA), it’s not yet approved for psoriasis. Some studies have demonstrated that it’s an effective psoriasis treatment.

TNF-a inhibitors

TNF-a is also a pro-inflammatory cytokine. Psoriatic lesions contain elevated levels of TNF-a.

There are several FDA-approved TNF-a inhibitors, such as:

  • etanercept (Enbrel)
  • infliximab (Remicade)
  • adalimumab (Humira)
  • certolizumab (Cimzia)

Other new treatments, and treatments on the horizon, for psoriasis include:

Tyrosine kinase 2 (TYK2) inhibitors

Like JAK proteins, TYK2 proteins are located within cells and are associated with receptors located on the cell surface. They can activate cellular signaling pathways when proteins such as IL-12 or IL-23 bind to the receptor. As such, inhibiting TYK2 activity could be beneficial in treating psoriasis.

One TYK2 inhibitor that’s currently undergoing safety and efficacy testing for psoriasis treatment is the small molecule BMS-986165. It binds to a specific part of the TYK2 protein, preventing the protein from functioning correctly.

A phase II clinical trial looked at people with moderate to severe plaque psoriasis. Results showed that oral BMS-986165 had few serious side effects and cleared psoriasis better than a placebo.

A phase III clinical trial is currently recruiting. In phase III, researchers will compare the effects of BMS-986165 against both a placebo and apremilast (Otezla).

Topical treatments

In addition to injectable and oral medications, researchers are also on the lookout for new topical treatments.

A Romanian study investigated the use of Dr. Michaels natural products in the treatment of mild to severe plaque psoriasis. Dr. Michaels products also sold under the brand name Soratinex.

Most participants observed a moderate to outstanding improvement when the products were applied to skin and scalp lesions twice a day. However, the treatment did cause side effects such as itching and hair follicle inflammation.

These new medical treatments are exciting, but they’re not all that’s happening in the field of psoriasis study. Researchers are trying to understand what the disease does inside a person’s body.

Psoriasis is an autoimmune disease. It occurs because your body’s immune system malfunctions. Your immune system is designed to detect, stop, and defeat invading bacteria and viruses. When you have an autoimmune disease, your immune system begins attacking healthy cells.

Researchers are trying to understand why autoimmune diseases develop. Studies into other autoimmune conditions will help people with psoriasis too. The more that’s known about autoimmune diseases, the better treatments and prognosis will be for everyone.

The following theories about the immune system’s role in the initiation of psoriasis have been proposed:

  1. Dendritic cells recognize proteins released by skin cells in response to injury, stress, or infection. A dendritic cell is a type of immune cell.
  2. The dendritic cells become active and begin secreting cytokines — such as IL-12 and IL-23 — that promote the growth and development of T cells. A T cell is another specific type of immune cell.
  3. The response of the T cells helps to drive the inflammation and skin cell growth associated with psoriasis.

A family history of psoriasis is one of the biggest risk factors for the condition. If one or both of your parents have psoriasis, your risk is significantly higher. Researchers have discovered a number of genes that are involved in passing the disease from one generation to the next.

Studies have identified a “psoriasis susceptibility” location on chromosome 6 of the human genome. Additional genetic risk factors have been identified throughout the human genome. The genes are associated with skin function and immune response.

However, not everyone with a family history of psoriasis will develop it. Researchers are trying to identify what increases a person’s likelihood of developing the disease and what might be done to stop parents from passing on these genes.

Researchers are also specifically looking at these areas:

Nervous system

Scaly red lesions and white-silver plaques are the most recognizable aspect of psoriasis. Pain and itching are also very common. Researchers are investigating what causes this pain and itching and what can be done to stop those sensations.

A recent study in a mouse model of psoriasis used chemical treatment to deplete sensory nerves associated with pain. The researchers found that the mice exhibited less inflammation, redness, and discomfort. This implies that sensory nerves may play a role in the inflammation and discomfort associated with psoriasis.

Skin-cell formation

If you have psoriasis, your immune system mistakenly attacks your skin cells. This causes skin cells to be produced very rapidly.

Your body has no time to naturally eliminate these cells, so lesions develop on the surface of your skin. Researchers hope that understanding how skin cells form will help them interrupt the process and stop uncontrolled skin-cell formation.

One recent study looked at how gene regulation differs between healthy skin cells and skin cells in psoriatic lesions. When compared to healthy skin cells, cell populations from psoriatic lesions saw a greater expression of genes associated with cell growth, inflammation, and an immune response.

Skin microbiome

A microbiome is made up of all of the microorganisms that occur in a specific environment. Investigators have recently become interested in how the different microbiomes of the human body, such as those in the digestive tract, may affect various diseases or conditions.

Could the microbiome of the skin play a role in psoriasis?

One recent study compared the microbes on the skin of healthy individuals to those on the skin of people with psoriasis. They found that the two microbial communities were very different.

The microbes found on the skin of people with psoriasis were more diverse and had more bacterial species, such as Staphylococcus aureus, that may lead to increased inflammation.

A comorbidity is when one or more additional conditions occur with a primary condition. People with psoriasis are at a greater risk of developing certain conditions. These include:

Researchers want to understand the relationship between psoriasis and these conditions in the hope of preventing them from occurring in people with psoriasis.

A 2017 study of nearly 470,000 Americans with psoriasis looked at the most prevalent comorbidities. The most common ones included:

  • high blood lipids
  • high blood pressure
  • depression
  • type 2 diabetes
  • obesity

All of these areas of research hold great promise. Still, progress won’t be accomplished overnight. Researchers and advocacy organizations work every day to discover new treatments for psoriasis.

In fact, in 2019, the National Psoriasis Foundation (NPF) organized their first Cure Symposium. The goal of this meeting was to bring together doctors and researchers to discuss ways to treat, prevent, and even cure psoriasis. The organizers hope that this meeting of the minds will aid in encouraging new advances or discoveries within the field.