In the 1960s and '70s, discovery of the immune system’s role in psoriasis led to several effective psoriasis treatments, among them corticosteroids, cyclosporine, and methotrexate. For the next few decades, though, treatment for psoriasis was mostly stuck in neutral.
Thanks to recent breakthroughs in psoriasis research, that’s ancient history. New biologic therapies are highly effective for treating psoriasis, although they’re expensive and carry some risk. Other new psoriasis treatments are also close to FDA approval, bringing hope to millions of psoriasis sufferers.
A New Era of Psoriasis Treatment
Research in psoriasis doesn’t make headlines -- or win funding -- like discoveries in cancer or heart disease. Also, psoriasis research is hamstrung by the uniqueness of human skin: Unlike in other diseases, experiments on mice or other animals aren’t very helpful.
In recent years, though, psoriasis research funding by the National Institutes of Health has doubled. More broadly, research into other autoimmune diseases has yielded new knowledge about the immune system. It turns out some of the problems in other autoimmune illnesses are active in psoriasis, as well.
This greater understanding of immune system diseases has brought new treatments, targeted at specific aspects of the immune system. Called biologic agents, these drugs have launched a new era of treatment for psoriasis.
Biologic Agents as Psoriasis Treatment
Biologic agents are medicines made from substances found in living organisms. These lab-manufactured proteins or antibodies are injected into the skin or bloodstream. Once inside the body, the drug blocks some part of the altered immune system that contributes to psoriasis.
In general, biologic agents improve psoriasis by:
- Suppressing T-cells (a form of white blood cell) directly
- Blocking a substance called tumor necrosis factor-alpha (TNF-alpha), one of the main messenger chemicals in the immune system
- Blocking a family of the immune system’s chemical messengers called interleukins
The patches and plaques of psoriasis result from a dysfunctional interaction between skin cells and white blood cells. By interfering with TNF-alpha or T-cells, or targeting proteins called interleukins, biologic agents short-circuit the unhealthy association between the two cell types. Inflammation (redness and itch) and the overgrowth of thick, scaly skin are both reduced.