Pain receptors in skin may trigger psoriasis
That painful feeling you get during a psoriasis flare may not just be a symptom of the disease. The same nerves responsible for the sensation of pain may also play an important role in triggering psoriasis.
A recent study published in Nature suggests that nociceptors, a kind of nerve ending that causes the perception of pain, help drive the inflammatory response that leads to psoriasis flares. The study's findings indicate that nociceptors, or pain fibers, control the function of immune cells in the skin.
Scientists have known for some time that communication between the nervous system and the immune system helps modulate immune response, said Dr. Lorena Riol-Blanco, a co-lead author of the study. But they hadn't fully figured out how this relationship works.
Riol-Blanco and her colleagues discovered that pain fibers drive skin inflammation by controlling the function of dendritic cells in the skin. These cells are a source of interleukin-23 (IL-23), a protein that helps regulate the immune system and contributes to inflammation.
Pain fibers tell dendritic cells to make IL-23, said Riol-Blanco, who was awarded a National Psoriasis Foundation grant to support this research. "This sets into motion a series of reactions that leads to new plaque flares," she explained.
The production of IL-23 triggers the production of interleukin-17 and interleukin-22, which, like IL-23, are immunoregulatory proteins. These proteins, also known as cytokines, produce keratinocytes, the skin cells that build up in psoriasis plaques.
Next up for the research team is investigating ways to intervene in the interactions between immune cells and nerves. Determining how to disrupt their lines of communication could ultimately lead to the development of more targeted treatment options.