Allergic and autoimmune disorders have long been considered opposing forms of immune dysfunction, traditionally evaluated and treated separately. But growing evidence is challenging that distinction, revealing shared underlying mechanisms that could change how clinicians evaluate, manage, and potentially prevent both types of disease.

As patients frequently present with co-occurring conditions, research shows both disease types may arise from shared inflammatory pathways, genetic susceptibilities, and potential environmental contributors such as everyday chemicals that disrupt the epithelial barrier in the skin, gastrointestinal, and respiratory tracts, and affect the microbiome.

This shift in understanding may "redefine the purpose of treating allergic and autoimmune conditions," said Giuseppe Alvise Ramirez, MD, PhD, an immunologist in the Department of Allergy, Immunology, Rheumatology, and Rare Diseases at Ospedale San Raffaele in Milan, Italy, who co-authored a  2025 review examining the overlap. "Not just inducing remission and preventing relapses of autoimmunity and allergy alone but rather silencing a more complex pathological process able to cause further disability in multiple ways."

The emerging understanding could also open new avenues for treatment. According to Ramirez, it has paved the way for repurposing medications developed for allergic diseases to treat autoimmune conditions, and vice versa, including therapies targeting interleukin-5 and Janus kinase signaling. The findings are also driving research into shared pathways of immune dysregulation that could yield new biomarkers and therapeutic targets.

Evidence of a Connection 

Recent research has found that allergic and autoimmune diseases frequently coexist.

A  2019 US cross-sectional study found that adults with atopic dermatitis were more likely to have an autoimmune disorder than those without it (7.9% vs 5.7%). The difference was also observed in children (2.0% vs 1.0%).

More recently, a  2025 systematic review and meta-analysis of 26 studies found a 49% higher hazard of autoimmune disease in patients with atopic dermatitis (HR, 1.49; 95% CI, 1.31-1.70). Autoimmune conditions studied included rheumatoid arthritis, systemic lupus erythematosus, celiac disease, alopecia areata, Sjögren syndrome, and ulcerative colitis.

A  2026 nationwide cohort study of more than 269,000 South Korean adults examined associations between asthma, allergic rhinitis, and atopic dermatitis and several autoimmune diseases. Allergic disease was associated with higher risks of six autoimmune outcomes — rheumatoid arthritis, Hashimoto's thyroiditis, Graves' disease, ankylosing spondylitis, ulcerative colitis and systemic lupus erythematosus.

The connection is also apparent in clinical practice, according to Rita Kachru, MD, section chief for clinical immunology and allergy at UCLA Health in Los Angeles, who said she frequently encounters patients with both allergic and autoimmune conditions.

Mechanics of the Connection

Allergic diseases have historically been associated primarily with T-helper 2 (Th2) immune responses, while autoimmune disorders have been linked more closely to Th1 responses.

However, this distinction is increasingly recognized as overly simplistic, Kachru said. Research suggests that the two types of disease share inflammatory signaling pathways and genetic susceptibility, as well as mechanisms that regulate immune tolerance.

Disruptions in these overlapping processes may interfere with the immune system's ability to distinguish harmless substances and the body's own tissues from genuine threats, potentially contributing to both allergic and autoimmune responses, according to Ramirez.

"When the immune system commits a mistake, the consequences are loss of immunological tolerance and misdirected inflammatory responses, either allergic or autoimmune," he said.

Kachru believes restoring immune tolerance could become an increasingly important focus of treatment.

"You're going to hear a lot in the next 15, 20 years about immune tolerance," she said. 

Ramirez has observed that patients with severe systemic lupus erythematosus often have allergies, including drug hypersensitivities, that develop during autoimmune flares. He also pointed to food allergy and celiac disease as another example of potential overlap, with both affecting the gastrointestinal tract, a potentially vulnerable site for immune dysfunction.

He suggested that persistent allergic or autoimmune inflammation may reinforce abnormal immune responses, potentially contributing to additional sensitivities over time.

Is the Epithelial Barrier the Missing Link? 

The epithelial barrier is increasingly recognized as an avenue through which immune dysregulation can occur. The barrier is the protective layer of cells lining the skin, respiratory tract, and gastrointestinal system.

Cezmi Akdis, MD, PhD, the director of the Swiss Institute of Allergy and Asthma Research in Davos, Switzerland, developed the epithelial barrier theory, which proposes that damage to these protective surfaces may contribute to the increasing prevalence of allergic and chronic inflammatory diseases, including some autoimmune conditions.

According to the theory, exposure to pervasive substances like cleaning surfactants, air pollutants, microplastics, and food emulsifiers can disrupt the tight junctions connecting epithelial cells, allowing allergens, pollutants, and microbes to interact more readily with immune cells. This may trigger persistent inflammation and interfere with the mechanisms that ordinarily prevent inappropriate immune responses, he said.

"Tolerance mechanisms are very important against environmental proteins or self-proteins," Akdis said. "Because of chronic inflammation, the tolerance mechanisms are mixed up. So we cannot tolerate our own tissues anymore. We cannot tolerate environmental proteins."

The theory also involves the microbiome, which plays an important role in immune regulation. Changes in the communities of microorganisms inhabiting epithelial surfaces may further promote inflammation and interfere with immune tolerance, Akdis said.

He recommends reducing unnecessary contact with substances that may damage epithelial barriers, such as certain surfactants found in household cleaners, dishwasher detergents, and personal care products.

What Should Clinicians Do Differently? 

Kachru said her team routinely evaluates patients with allergic disease for symptoms and family histories suggestive of autoimmunity. She recommends asking about gastrointestinal symptoms, unexplained rashes, recurrent fevers, and photosensitivity, with laboratory testing guided by clinical suspicion.

"You can't have a clinical suspicion if you haven't asked about it," Kachru said. "Patients don't necessarily link them together and won't know to tell you unless you ask."

Ramirez said the emerging evidence could eventually change how clinicians approach both disease categories. Identifying shared immune abnormalities and biomarkers may help guide more targeted treatments, moving beyond managing allergic and autoimmune conditions as separate diseases.

"Therapeutic advances in immunology are rapidly moving towards immune-editing strategies promising to fine-tune the inflammatory response at a cellular and molecular level," he said.

Ramirez, Kachru, and Akdis reported no conflicts of interest.