Asthma is not classified as an autoimmune disease. It is officially categorized as a chronic inflammatory airway disease, and the 2024 Global Initiative for Asthma (GINA) report describes it as a heterogeneous condition with multiple distinct phenotypes, including allergic, nonallergic, and cough-variant forms. However, the line between asthma and autoimmunity is blurrier than it used to be, and recent genetic and immunological research suggests the two conditions share more biology than previously thought.
Why Asthma and Autoimmunity Were Considered Opposites
For decades, immunologists placed asthma and autoimmune diseases on opposite ends of a seesaw. The immune system uses different “branches” to fight different threats. Autoimmune diseases like rheumatoid arthritis, lupus, and type 1 diabetes were thought to result from an overactive Th1 response, the branch that targets infected cells and, when misdirected, attacks your own tissues. Asthma, by contrast, was considered a Th2 problem: the branch that responds to parasites and allergens, producing the inflammation, mucus, and airway narrowing that define an asthma attack.
Under this model, the two branches counterbalanced each other. Ramping up one would suppress the other. A person prone to autoimmunity shouldn’t also be prone to allergic asthma, and vice versa. This clean framework shaped how both conditions were diagnosed, studied, and treated for years.
Where That Framework Breaks Down
The seesaw model hasn’t held up well. Large genetic studies have found that asthma and autoimmune diseases share common risk genes. Several gene regions previously linked to asthma susceptibility, including variants near immune signaling pathways, also increase the risk of autoimmune conditions. The effect goes in the same direction: the same genetic variant that raises your odds of asthma also raises your odds of autoimmune disease, not the opposite.
There’s also growing evidence that eosinophils, the immune cells most associated with allergic asthma, play a contributing role in certain autoimmune diseases. Meanwhile, the Th17 pathway, which drives many autoimmune conditions, has been implicated in some forms of severe asthma. The neat division between “asthma immune cells” and “autoimmune immune cells” is fading.
One emerging theory, called the epithelial barrier hypothesis, proposes that damage to the body’s surface barriers (in the skin, gut, or airways) can trigger both allergic and autoimmune diseases through similar mechanisms. The idea is that a compromised barrier lets environmental substances interact with the immune system in ways that push it toward chronic, misdirected inflammation, regardless of whether the end result looks like asthma or an autoimmune condition.
Autoantibodies in Severe Asthma
One hallmark of autoimmune disease is the presence of autoantibodies: immune proteins that mistakenly target your own tissues. Researchers have recently found that some people with severe eosinophilic asthma produce autoantibodies at rates significantly higher than healthy people. A study published in Frontiers in Immunology identified elevated autoantibodies targeting collagen-V (a structural protein in the lungs), myeloperoxidase (an enzyme in immune cells), and a receptor on immune cells called TREM1 in patients with severe eosinophilic asthma compared to healthy controls.
This doesn’t prove that asthma is autoimmune, but it does suggest that in its most severe forms, the immune dysfunction in asthma starts to resemble autoimmunity. Regulatory T cells, which act as brakes on the immune system, also appear to function poorly in asthma, a feature shared with several established autoimmune disorders.
Asthma and Autoimmune Disease Overlap in Real Patients
If asthma and autoimmunity were truly opposite conditions, you wouldn’t expect to see them in the same people very often. But they co-occur more than chance would predict. People with lupus develop asthma at roughly 2.5 times the rate of people without lupus, with an incidence of about 23 per 10,000 person-years compared to 8 per 10,000 in the general population. That elevated risk holds even after adjusting for age, sex, and other health factors.
The overlap extends to rheumatoid arthritis. A large analysis of Korean national health insurance data found that adults with asthma had about 59% higher odds of also having rheumatoid arthritis compared to adults without asthma. Tumor necrosis factor-alpha, a key inflammatory molecule, has been identified as a shared genetic risk factor for asthma, juvenile rheumatoid arthritis, and lupus.
How Asthma Is Diagnosed Differently
Despite the biological overlap, asthma is diagnosed through entirely different tests than autoimmune diseases. Autoimmune screening typically involves blood tests looking for autoantibodies and markers of systemic inflammation. Asthma diagnosis relies on lung function.
The core test is spirometry, which measures how much air you can blow out and how quickly. You breathe into a device, then inhale a bronchodilator (a medication that relaxes airway muscles) and blow again. If your airflow improves significantly after the bronchodilator, that reversibility is a strong sign of asthma. A ratio of forced expiratory volume to total lung capacity below 0.75 in adults points toward obstruction.
Doctors may also measure fractional exhaled nitric oxide (FeNO), a gas that increases when your airways are inflamed. Levels above 50 parts per billion in adults suggest eosinophilic airway inflammation that typically responds well to steroids. Levels below 25 ppb point toward asthma without eosinophilic inflammation, which may need a different treatment approach. None of these tests look for the autoantibodies or immune markers that define autoimmune conditions.
How Flares Differ
Asthma exacerbations and autoimmune flares feel and behave differently, even though both stem from immune dysfunction. An asthma flare is centered in the airways: wheezing, chest tightness, coughing, shortness of breath. It’s often triggered by something identifiable, like pollen, cold air, exercise, or a respiratory infection. The response is relatively fast, developing over minutes to hours, and can usually be reversed with a rescue inhaler.
Autoimmune flares tend to be systemic, meaning they affect multiple body systems at once. Lupus flares might involve joint pain, fatigue, skin rashes, and kidney problems. Rheumatoid arthritis flares center on joint swelling and stiffness. These episodes build over days to weeks, don’t respond to bronchodilators, and typically require immunosuppressive medications to bring under control. The distinction matters practically: the triggers, the timeline, and the treatments are different even when the underlying immune dysfunction shares genetic roots.
Shared Treatment Strategies
Where asthma and autoimmune disease do converge practically is in treatment. Both conditions are managed by calming an overactive immune system, and some of the same biologic medications are now approved for conditions on both sides of the old divide.
Mepolizumab, which targets a protein that drives eosinophil production, is approved for severe asthma but also for eosinophilic granulomatosis with polyangiitis (EGPA), a condition that sits squarely in autoimmune territory. Benralizumab, which works on the same pathway by targeting the receptor on eosinophils directly, is also approved for both severe asthma and EGPA. Dupilumab, which blocks two inflammatory signaling molecules, is used for severe asthma, atopic dermatitis, and eosinophilic esophagitis.
The fact that the same drugs work across these conditions reinforces the idea that asthma and autoimmune diseases aren’t opposite problems. They’re different expressions of immune systems that have lost the ability to regulate themselves properly, sometimes through the very same molecular pathways.
The Bottom Line on Classification
Asthma is not currently classified as an autoimmune disease, and for most people with mild to moderate allergic asthma, the distinction holds: their immune systems are overreacting to external allergens, not attacking their own tissues. But severe asthma, particularly the eosinophilic subtype, shows autoimmune-like features including autoantibodies, regulatory T cell dysfunction, and shared genetic risk factors with established autoimmune conditions. The boundaries between these categories are far less clear than they appeared a generation ago, and the immune system doesn’t seem to respect the neat boxes that medical classification prefers.