This test is most useful if any of these apply to you.
IL-17 helps drive inflammation in psoriasis and several forms of inflammatory arthritis. Its role in these diseases is well established. Measuring its concentration in your blood has a less established role: it hasn't been validated as a routine way to diagnose these conditions, choose treatment, or detect disease before symptoms appear.
Blood IL-17 remains an exploratory biomarker for prevention and routine disease monitoring. Studies have found associations with disease activity and outcomes, but results vary across conditions and laboratories. There are no universally accepted clinical decision limits, and collecting a personal trend hasn't been shown to improve health outcomes.
IL-17 belongs to a family of signaling proteins called cytokines. These proteins carry instructions between cells. The name IL-17 commonly refers to IL-17A, although the family contains several distinct proteins. IL-17F is a closely related member that can pair with IL-17A.
Th17 cells are one source of IL-17A. They are a type of white blood cell, and several other immune cell populations can produce it too. Another cytokine, IL-23, helps maintain some of these responses, but IL-17 production can also occur without IL-23.
IL-17 acts on cells in tissues such as the skin and airways, prompting them to release antimicrobial proteins and signals that recruit neutrophils. Neutrophils are white blood cells that respond quickly to infection. This response helps protect against Candida yeast and certain bacteria, but sustained activation can contribute to tissue inflammation and damage.
Rare inherited defects affecting IL-17 signaling can cause persistent or recurring Candida infections of the mouth, skin, and nails. Those disorders involve how the immune system produces or responds to signals. A circulating IL-17 concentration does not establish whether that defense is functioning normally.
This test reports a blood concentration in pg/mL. The supplied test information does not specify whether the laboratory uses serum or plasma, or which measurement method it uses. Serum and plasma are liquid portions prepared from blood in different ways. Results from these specimens and from different laboratory methods aren't automatically interchangeable.
The studies below identify serum or plasma where the source specifies it. Findings about IL-17 in skin, saliva, spinal fluid, or isolated immune cells describe related biology, but they cannot be treated as measurements of the same thing. The amount circulating in blood also doesn't directly measure IL-17 activity inside a particular joint or skin lesion.
Research has found higher circulating IL-17 in groups with psoriasis, rheumatoid arthritis, and other inflammatory conditions. Whether it tracks activity within an individual is less consistent. Evidence that the IL-17 pathway contributes to disease does not establish that its blood concentration can diagnose that disease or reliably measure its severity.
One study found average plasma IL-17A more than eleven times higher in people with rheumatoid arthritis than in healthy controls, with higher concentrations associated with greater disease activity. Another study found that serum IL-17A identified about 81% of moderate-to-high activity cases and correctly classified about 84% of low-activity cases. Those results came from selected study groups; they have not established a diagnostic or monitoring rule for your laboratory result.
In that second study, combining IL-17A with TNF-alpha improved some measures of classification within the study population. TNF-alpha is another inflammatory cytokine. The combination still needs independent validation before it can be used as a routine arthritis assessment.
Lupus illustrates why a higher group average can be misleading. A study of 98 people found higher serum IL-17 than in healthy controls, but levels did not correlate with standard measures of disease activity, including during follow-up. An association with nervous-system involvement was observed. A separate small study linked circulating IL-17 to lupus kidney disease activity, but these findings do not establish dependable monitoring across all forms of lupus.
The cardiovascular research does not support a simple higher-is-worse interpretation. Lower circulating IL-17 was associated with worse outcomes after a heart attack, while higher concentrations were associated with worse outcomes in heart failure and intensive care.
| Who Was Studied | Measurement | What They Found |
|---|---|---|
| 981 adults hospitalized for a heart attack, followed for two years | Serum IL-17 below versus above the study group's midpoint | The lower group had about a 40% higher rate of death or another heart attack after adjustment for other risk factors. |
| 3,819 adults across two heart-failure cohorts | Serum IL-17 | Higher concentrations were associated with more severe heart failure and higher mortality after adjustment. Associations with the combined outcome of death or hospitalization were weaker after adjustment. |
| 299 adults in intensive care | Serum IL-17A | Higher concentrations were associated with hospital mortality and adverse kidney outcomes. |
These studies examined different illnesses and stages of disease. They cannot establish that raising IL-17 after a heart attack would help, or that lowering it in heart failure would improve survival. They also did not test whether using the result to guide care improves outcomes.
Chronic obstructive pulmonary disease is usually shortened to COPD. A pooled analysis found higher serum IL-17 in people with COPD than in healthy controls, and higher concentrations during exacerbations than during stable disease. Individual studies differed, and the analysis did not establish a blood test that can replace breathing tests or clinical assessment.
In a study of 2,391 children hospitalized with Mycoplasma pneumoniae pneumonia, circulating IL-17 was higher in severe and treatment-resistant cases. A separate study of 165 adults in intensive care found that serum IL-17 helped distinguish sepsis from localized infection, particularly when combined with IL-10 and procalcitonin. These were hospital-based research findings, not validated screening strategies for otherwise well adults.
Infection is therefore one possible explanation for a change in IL-17. These studies do not establish how every minor infection affects the result or how long a change persists after recovery.
Some studies in people with diagnosed cancer have linked higher circulating IL-17 to shorter survival. In a meta-analysis of Chinese lung-cancer studies, the serum-only subgroup had about 2.4 times the rate of death in the higher-IL-17 group. The full analysis also included measurements from other specimens, so its results should not all be attributed to blood testing.
A bladder-cancer meta-analysis also associated higher serum IL-17 with shorter survival. Its IL-17 evidence came from only two studies totaling 124 people, although the larger review included many more people studied for IL-6. The pooled mortality estimate was about 3.3 times higher, with substantial uncertainty. It should not be used to estimate your personal prognosis.
Studies of Th17 cell proportions have sometimes found better survival with higher proportions, while studies of circulating IL-17 protein have often found the opposite or no clear association. Counting a particular immune-cell population and measuring the protein released by several cell types are different measurements.
These findings concern prognosis after cancer has been diagnosed. They do not validate IL-17 as a cancer screening test.
A small human study found higher serum IL-17A in people with mild cognitive impairment or early Alzheimer's disease than in controls. Measurements in cerebrospinal fluid moved in a different direction. Cerebrospinal fluid surrounds the brain and spinal cord. The study does not establish that a blood IL-17 result measures inflammation in your brain, detects a leaky blood-brain barrier, or predicts future dementia.
Biological variation and laboratory variation both matter. Small repeated-sampling studies have documented fluctuations in circulating IL-17A, but they do not provide a universal percentage change that proves a meaningful shift. At low concentrations, results may also approach a method's detection limit, where measurement uncertainty becomes more important.
Repeated measurements can document whether the concentration changes under consistent conditions. They do not, by themselves, establish why it changed or whether your health improved. Some disease studies show associations with activity; others show little relationship or persistent elevation despite clinical recovery.
For an individual result to guide treatment, a change would need to predict something useful beyond symptoms, examination findings, and established tests. That role remains unproven for routine blood IL-17 monitoring, particularly in healthy people.
Evidence-backed interventions that affect your IL-17 level
IL-17 is best interpreted alongside these tests.