We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.


Blocking Inflammatory Protein May Delay Skin Aging

An older woman's hands.
Credit: Eduardo Barrios/Unsplash

Want a FREE PDF version of this news story?

Complete the form below and we will email you a PDF version of "Blocking Inflammatory Protein May Delay Skin Aging"

Listen with
Register for free to listen to this article
Thank you. Listen to this article using the player above.

Want to listen to this article for FREE?

Complete the form below to unlock access to ALL audio articles.

Read time: 2 minutes

Researchers have shown that the inflammatory molecule IL-17 has a key function in skin aging. The study was published in Nature Genetics by a team of researchers from the Institute for Research in Biomedicine (IRB Barcelona) working alongside the National Center for Genomic Analysis (CNAG).

How our skin ages

The aging process in the skin is accompanied by changes to how skin cells function and connect that over time lead to vulnerability. Old skin is more fragile and is less able to heal once damaged. Skin is a jumble of interconnected cell types, including epithelial cells, hair follicles and immune cells. Their presence in the skin is essential to protecting the body from external threats and infection. Some of these cells, such as CD4+ T cells, fire out chemicals called cytokines that amplify immune processes. The scientists’ interest in IL-17 was piqued by the observation that cells producing it become more common and more active in older skin. Now, researchers have tied increased levels of IL-17 to the processes underlying age-related skin deterioration.

Want more breaking news?

Subscribe to Technology Networks’ daily newsletter, delivering breaking science news straight to your inbox every day.

Subscribe for FREE

“Our results show that IL-17 is involved in various functions related to aging. We have observed that blocking the function of this protein slows down the appearance of various deficiencies associated with aging skin. This discovery opens up new possibilities for treating some of the symptoms or facilitating skin recovery after surgery, for example,” explains Dr. Aznar Benitah, head of the Stem Cells and Cancer Laboratory at IRB Barcelona.

Dr. Holger Heyn, head of the Single Cell Genomics laboratory at CNAG, adds, “Single cell sequencing has allowed us to dive deep into the complexity of cell types and states forming the skin and how these change during lifespan. We did not only find differences in the composition of aged skin, but also changes in cell activity states. Particularly immune cells showed specific age-related profiles, which we could pinpoint by analyzing thousands of individual cells one at a time.”

IL-17 and autoimmune disease

IL-17 has been previously linked to autoimmune skin conditions, such as psoriasis. Existing treatments for this condition, such as the antibody secukinumab, act by blocking IL-17. The team explored the effect of blocking the protein on a series of skin aging measures, including hair follicle growth, rate of water loss, healing ability and genetic markers. Blocking Il-17 led to improvements in all four categories. Nevertheless, say the authors, Il-17’s role in immunity means that permanently blocking it could have dangerous side effects. Instead, they believe the temporary block they have demonstrated in the current study could be a way forward for anti-aging treatments.

The mechanisms that link IL-17 block to delayed aging processes are still unclear. In future research, the team state that they want to clarify these processes and address how IL-17 may be linked to aging in other organs.

Reference: Solá P, Mereu E, Bonjoch J, et al. Targeting lymphoid-derived IL-17 signaling to delay skin aging. Nat Aging. Published online June 8, 2023:1-17. doi:10.1038/s43587-023-00431-z 

This article is a rework of a press release issued by IRB Barcelona. Material has been edited for length and content.