Endometriosis is not currently classified as an autoimmune disease, but it shares a striking number of features with autoimmune conditions. It involves chronic inflammation, immune system dysfunction, and the presence of autoantibodies. The medical community increasingly views it as an immune-related disorder, and women with endometriosis are roughly twice as likely to be diagnosed with a recognized autoimmune disease compared to women without it.
Why the Confusion Exists
Autoimmune diseases share a basic pattern: the immune system mistakenly attacks the body’s own tissue, causing chronic inflammation and damage. Endometriosis checks several of those boxes. Tissue similar to the uterine lining grows outside the uterus, and the immune system fails to clear it. Inflammatory markers spike. Antibodies appear that target the body’s own cells. This overlap is why researchers have debated the classification for decades.
But endometriosis doesn’t fit the autoimmune label cleanly. In classic autoimmune diseases, the immune system is overactive, directly destroying healthy tissue. In endometriosis, the problem is partly the opposite: certain immune cells are underperforming, allowing misplaced tissue to survive and spread. It’s less that the immune system is attacking itself and more that it’s failing to do its job while simultaneously driving inflammation. That distinction keeps endometriosis in a gray zone, officially categorized as a chronic inflammatory gynecological condition rather than a true autoimmune disease.
Immune Dysfunction in Endometriosis
Nearly all immune cell types in women with endometriosis show functional abnormalities. The most well-documented involves natural killer (NK) cells, which are part of the body’s first line of defense. Normally, NK cells would recognize and destroy tissue growing where it shouldn’t be. In endometriosis, these cells are present but essentially disabled.
The dysfunction works on multiple levels. NK cells in the pelvic cavity of women with endometriosis show reduced levels of a key recognition receptor, limiting their ability to identify misplaced endometrial cells. At the same time, they ramp up production of an inhibitory receptor that actively suppresses their killing ability. The result is a population of immune cells that can find the problem but can’t act on it. This mirrors immune escape pathways seen in cancer, where tumors evolve ways to shut down the immune cells trying to eliminate them.
The misplaced endometrial cells also play an active role in their own survival. They release a soluble molecule that blocks NK cells from forming a stable physical connection with their target, essentially preventing the immune cell from latching on and delivering its toxic payload. They also display surface proteins that send “don’t kill me” signals to approaching immune cells. Together, these mechanisms create an environment where rogue tissue persists and grows, fueling a cycle of inflammation.
Autoantibodies and Inflammatory Markers
Women with endometriosis produce autoantibodies at higher rates than the general population. About 60% of patients with endometriosis have detectable antibodies targeting endometrial tissue. In one study, 21.2% of endometriosis patients tested positive for antinuclear antibodies (a hallmark of autoimmune disease) compared to just 5.4% of controls. These are the same antibodies doctors test for when screening for lupus or rheumatoid arthritis.
The inflammatory picture is equally telling. Levels of a key inflammatory signaling molecule (interleukin-6) in the pelvic fluid of women with endometriosis average around 797 pg/ml, roughly six times higher than the 133 pg/ml found in women without the condition. Levels of an immune-suppressing molecule (interleukin-10) are also nearly doubled. This combination of heightened inflammation alongside increased immune suppression is a hallmark of the disease and helps explain why endometriosis tissue both provokes pain and avoids destruction.
The Autoimmune Disease Connection
A large case-control study of nearly 200,000 endometriosis patients found that about 5% received a diagnosis of at least one autoimmune condition within two years of their endometriosis diagnosis. That rate was approximately double what researchers saw in matched controls. The elevated risk wasn’t limited to one or two conditions. It spanned a wide range of autoimmune diseases.
The strongest associations were with Sjögren’s syndrome (3.4 to 5 times higher odds), an inflammatory muscle disease called myositis (3.8 to 5.9 times higher), and pernicious anemia (2.4 to 3.6 times higher). Rheumatoid arthritis, Hashimoto’s thyroid disease, lupus, and multiple sclerosis all showed roughly 2 to 3 times higher odds among endometriosis patients. Even type 1 diabetes and Graves’ disease appeared at modestly elevated rates.
What researchers don’t yet know is the direction of this relationship. Endometriosis might predispose women to autoimmune conditions, autoimmune processes might make endometriosis more likely, or both types of disease might stem from shared underlying mechanisms. The co-occurrence is consistent enough, though, that if you have endometriosis and develop new symptoms like joint pain, extreme fatigue, dry eyes and mouth, or unexplained thyroid changes, those symptoms are worth investigating.
What This Means for Treatment
Standard endometriosis treatment focuses on surgery to remove misplaced tissue and hormonal therapy to suppress ovarian function, both of which address the disease without targeting the immune dysfunction driving it. The recognition that endometriosis has a strong immune component has prompted research into treatments borrowed from autoimmune medicine.
Drugs that block a specific inflammatory protein called TNF-alpha have shown promise in laboratory and early clinical studies. These agents can reduce the ability of pelvic fluid from endometriosis patients to stimulate the growth of endometrial cells. Some existing endometriosis medications already have immune-modulating effects that weren’t initially recognized. Danazol, a synthetic hormone used for endometriosis since the 1970s, turns out to suppress inflammatory signaling molecules produced by immune cells and inhibit the proliferation of certain immune cells activated in the disease.
None of the immune-targeted therapies have become standard care yet. But the direction of research is clear: treating endometriosis as purely a hormonal or surgical problem misses a significant piece of the puzzle. The immune dysfunction isn’t a side effect of the disease. It’s central to how endometriosis establishes itself, persists, and causes pain.
A Disease That Defies Simple Categories
The honest answer to whether endometriosis is autoimmune is that it doesn’t fit neatly into existing categories. It has autoimmune features: autoantibodies, chronic inflammation, tissue damage, and strong associations with recognized autoimmune diseases. But its core mechanism involves immune suppression and evasion rather than direct autoimmune attack. Some researchers have proposed reclassifying it as an autoimmune or autoimmune-related condition, though no major medical organization has done so.
What matters practically is that endometriosis is an immune-mediated disease, regardless of the label. The immune system is not a bystander. It is actively involved in allowing the disease to take hold and progress. If you have endometriosis and are also dealing with symptoms that suggest autoimmune activity, that overlap is well-documented and not coincidental.