Autoimmune diseases are not contagious. You cannot catch one from another person through physical contact, shared food, airborne droplets, or any other form of transmission. Unlike infections caused by bacteria or viruses, autoimmune diseases originate from a malfunction inside a person’s own immune system, not from an outside pathogen that spreads between people.
This is a reasonable question, though, because infections and autoimmune diseases can look similar on the surface. Both involve inflammation, both can cause fatigue and pain, and some autoimmune diseases are even triggered by infections. Here’s why the diseases themselves still can’t be passed along.
Why Autoimmune Diseases Can’t Spread
For a disease to be contagious, it needs a pathogen (a virus, bacterium, fungus, or parasite) that can leave one person’s body and establish itself in another. Autoimmune diseases don’t have one. Instead, they start when the immune system loses its ability to tell the difference between the body’s own cells and foreign invaders. Immunologists call this a breakdown of “immunological tolerance.”
Normally, your body has a quality-control process. During development, immune cells that would react against your own tissues are identified and eliminated. When that screening fails, rogue immune cells survive and eventually begin attacking healthy organs, joints, nerves, or skin. The result is chronic inflammation directed inward, not an infectious agent that could jump to someone else. Even if you were in close contact with a person who has lupus, rheumatoid arthritis, type 1 diabetes, or multiple sclerosis, there is nothing being produced in their body that could cause your immune system to malfunction in the same way.
The Infection Connection That Causes Confusion
One reason people wonder about contagiousness is that certain infections can act as triggers for autoimmune disease. Epstein-Barr virus (the virus behind mono) is linked to multiple sclerosis, and hepatitis C has been associated with several autoimmune conditions. But there’s a critical distinction: the virus itself may be contagious, while the autoimmune disease it occasionally triggers is not. The National Multiple Sclerosis Society states this plainly: “While the viruses that are potentially involved in the development of MS are infectious, MS itself is not.”
The mechanism behind this is called molecular mimicry. Some bacteria and viruses have surface proteins that look structurally similar to proteins on your own cells. After your immune system learns to attack the invader, it may accidentally start targeting the look-alike proteins on healthy tissue. Think of it as a case of mistaken identity that persists long after the original infection is gone. Research in animal models has shown that a virus carrying proteins similar to brain tissue couldn’t cause autoimmune disease on its own. The animals only developed disease after a second immune trigger, suggesting that mimicry loads the gun but doesn’t pull the trigger by itself.
Other paths exist too. Prolonged infections with viruses like Epstein-Barr or hepatitis C can keep immune cells in a state of constant activation, eventually producing antibodies that turn against the body. And sometimes an infection causes enough tissue damage that previously hidden proteins are exposed to the immune system for the first time, sparking a new autoimmune reaction. In every case, the autoimmune disease that results is an internal process, not something that can be transmitted.
What Actually Determines Your Risk
If autoimmune diseases aren’t caught from others, what causes them? The answer is a combination of genetics, environment, and immune system quirks that vary from person to person.
Genetics plays a substantial role. The heritability of rheumatoid arthritis is estimated at about 60%, meaning more than half the variation in who develops it can be traced to inherited factors. Identical twins of people with rheumatoid arthritis have a significantly higher concordance rate than the general population, with roughly a 3.7-fold increased risk. But genetics alone isn’t destiny. If it were, identical twins would always share the same autoimmune conditions, and they don’t.
Environmental factors fill in the rest. Smoking, vitamin D deficiency, hormonal shifts, chronic stress, and certain dietary patterns all influence risk. The gut microbiome also plays a surprisingly large role. Specific bacteria in your digestive tract produce compounds that either calm or provoke immune activity. For instance, certain beneficial gut bacteria produce short-chain fatty acids (especially butyrate) that strengthen the regulatory immune cells responsible for keeping autoimmunity in check. Other gut bacteria produce a compound called polysaccharide A that promotes anti-inflammatory signaling in the intestines. When this microbial balance tips in the wrong direction, the immune system can become more prone to attacking the body’s own tissues.
Why Autoimmune Patients Get More Infections
Another source of confusion: people with autoimmune diseases often seem to get sick more frequently. This can create the impression that something contagious is involved. In reality, the explanation is their treatment, not their disease.
Many autoimmune conditions are managed with immunosuppressant medications that deliberately dial down immune activity to stop the body from attacking itself. The tradeoff is that a suppressed immune system is also less effective at fighting off genuine threats. People on these medications face higher risks of respiratory infections (colds, flu, pneumonia), skin infections, fungal infections like thrush, and in serious cases, blood infections like sepsis. They are more likely to catch infections from others, not to give their autoimmune disease to others.
This is an important practical distinction. If someone you live with has an autoimmune condition and is on immunosuppressive therapy, they need protection from you when you’re sick, not the other way around. Standard precautions like hand washing and staying home when you have a cold or flu matter more in these households.
Autoimmune Diseases That Commonly Raise This Question
Some autoimmune conditions prompt this question more than others, usually because their symptoms are visible or because they share names or features with infectious diseases.
- Psoriasis: The red, scaly patches on the skin can look alarming, but psoriasis is caused by an overactive immune response that speeds up skin cell production. It is not a skin infection and cannot spread through touch.
- Rheumatoid arthritis: Joint swelling and deformity sometimes lead people to wonder if a germ is involved. The inflammation comes from immune cells attacking the joint lining, not from bacteria or viruses in the joint.
- Multiple sclerosis: Because viral infections like Epstein-Barr are linked to MS risk, some people assume MS itself is viral. It is not. The damage occurs when the immune system strips away the protective coating on nerve fibers in the brain and spinal cord.
- Type 1 diabetes: The immune system destroys insulin-producing cells in the pancreas. It sometimes appears in clusters within families, which can look like transmission, but the clustering reflects shared genetics, not contagion.
- Lupus: Lupus can affect the skin, joints, kidneys, and other organs. Its wide range of symptoms sometimes mimics infectious diseases, but the underlying cause is always the immune system targeting the body’s own tissues.
In every one of these conditions, the disease process is entirely internal. No autoimmune disease has ever been shown to pass from one person to another through any route of transmission.