IL-17 is a signaling protein produced by immune cells that acts as a bridge between your body’s adaptive immune system and its first-line inflammatory defenses. Its primary job is to recruit and activate neutrophils, a type of white blood cell that fights off bacteria and fungi. When IL-17 works correctly, it protects you from infections. When it’s overproduced or misdirected, it drives chronic inflammation in conditions like psoriasis, rheumatoid arthritis, and multiple sclerosis.
How IL-17 Works in the Body
IL-17 (formally called IL-17A) is the founding member of a family of six related proteins, labeled IL-17A through IL-17F. It’s produced mainly by a specialized group of immune cells called Th17 cells, which also release IL-17F and IL-22. These proteins trigger a broad tissue response because their receptors are found on cells throughout the body, not just in immune tissue.
When Th17 cells release IL-17, it sets off a cascade: target cells produce inflammatory signals like IL-6, chemokines that pull neutrophils to the site of trouble, and antimicrobial peptides that can directly kill pathogens. Think of IL-17 as a dispatch signal. It doesn’t kill invaders itself but coordinates the rapid arrival of cells and chemicals that do.
IL-17A and IL-17F are the two most studied members of the family. IL-17A is the more potent inflammatory trigger on its own, but neither works in isolation. Both dramatically amplify their effects when they team up with other inflammatory molecules like TNF-alpha and IL-1-beta. This synergy is part of what makes IL-17 so effective at fighting infections, and so destructive when it goes wrong.
IL-17’s Role in Fighting Infection
IL-17 plays a surprisingly specific role in defending against the fungus Candida albicans, a microorganism that naturally lives in your mouth, gut, and reproductive tract. At mucosal surfaces, IL-17 triggers a protective wave of neutrophil recruitment and antimicrobial peptide production that keeps Candida from overgrowing and shifting into its more invasive form. Oral and skin Candida infections are strongly dependent on IL-17 for control. In mice engineered to lack IL-17 signaling, susceptibility to both localized and systemic Candida infections increases significantly.
The antimicrobial peptides IL-17 induces, particularly a group called defensins, have direct antifungal activity. IL-17 also stimulates salivary gland cells to produce histatins, another class of antifungal proteins found in saliva. This layered defense explains why blocking IL-17 with medications can sometimes lead to yeast infections as a side effect.
When IL-17 Drives Disease
The same inflammatory power that makes IL-17 effective against infections can cause serious damage when Th17 cells activate inappropriately or excessively. Elevated IL-17 levels are found in the blood and tissue biopsies of people with rheumatoid arthritis, lupus, psoriasis, multiple sclerosis, inflammatory bowel disease, and several rarer conditions.
In psoriasis, both IL-17A and IL-17F contribute to the excessive skin cell turnover that creates thick, scaly plaques. Interestingly, IL-17F is found at concentrations up to 30 times higher than IL-17A in affected skin and blood, even though IL-17A is the more potent inflammatory signal per molecule. These elevated IL-17F levels also appear in psoriatic arthritis and other inflammatory conditions.
In multiple sclerosis, IL-17A is detectable in the cerebrospinal fluid, and Th17 cells that react to myelin (the protective coating on nerve fibers) are found in higher numbers. In Crohn’s disease, significantly more IL-17-producing cells cluster in inflamed gut tissue compared to healthy areas of the same patient’s intestine. In rheumatoid arthritis, IL-17A protein levels in joint fluid can be more than 37 times higher than IL-17F levels, a pattern that flips compared to what’s seen in skin disease.
Medications That Block IL-17
Three FDA-approved biologic drugs target the IL-17 pathway, all used primarily for moderate-to-severe psoriasis. Secukinumab, approved in 2015, is a fully human antibody that neutralizes IL-17A directly. Ixekizumab, approved in 2016, works the same way. Both are also approved for psoriatic arthritis and ankylosing spondylitis, a type of inflammatory spinal arthritis. Brodalumab, the newest of the three, takes a different approach by blocking the IL-17 receptor itself rather than the cytokine, and is approved strictly for psoriasis.
Because IL-17 is essential for antifungal defense, yeast infections are a known side effect. In a meta-analysis of 11 clinical trials covering over 7,300 patients on IL-17 inhibitors, candidiasis occurred in about 1.5% of treated patients. Most cases were mucosal (mouth or esophagus) rather than deep or life-threatening infections. Before starting treatment, doctors typically screen for signs of underlying inflammatory bowel disease, since blocking IL-17 can worsen gut inflammation. Patients with confirmed intestinal inflammation are generally steered toward other drug classes instead.
IL-17 and Heart Disease Risk
People with psoriasis and psoriatic arthritis already face higher cardiovascular risk, and IL-17A has been linked to processes that promote atherosclerosis. In animal studies, blocking IL-17A reduces plaque buildup, inflammatory cell infiltration, and lesion development in blood vessels. IL-17A also appears to promote new blood vessel growth within plaques and plaque hemorrhage, both of which make cardiovascular events more likely.
Whether IL-17 inhibitors translate these benefits to real patients is less clear. Two clinical trials examining secukinumab’s effect on blood vessel health found a neutral to mildly beneficial impact on artery function and aortic inflammation. However, a meta-analysis of nine randomized controlled trials found no statistically significant change in the rate of major cardiovascular events (heart attacks, strokes, cardiovascular death) in patients taking IL-17 inhibitors compared to placebo. There was also no dose-dependent effect. For now, IL-17 inhibitors don’t appear to raise or lower cardiovascular risk in a meaningful way.