A common strep throat infection can trigger guttate psoriasis, a sudden skin inflammation condition, by altering how key immune cells behave in the body. Researchers at Karolinska Institutet analyzed blood and skin samples from patients using advanced single-cell technology and discovered that neutrophils, the most abundant type of white blood cell, change their function during a streptococcal infection in ways that can lead to skin disease. What Are These Special Immune Cells Doing? The breakthrough centers on a previously unknown group of neutrophils with the ability to present antigens, which are fragments of pathogens that signal and guide other immune cells. During a strep infection, these antigen-presenting neutrophils accumulate in the affected skin of people with guttate psoriasis and activate T cells, which may contribute to inflammation. "Doctors have long known that strep throat can precede guttate psoriasis, but the biological explanation has been unclear," explains Avinash Padhi, first author of the study and Research Specialist at the Department of Medicine, Solna. "Our findings suggest a link between infection and skin inflammation through the accumulation of antigen-presenting neutrophils in patients' skin." The research challenges traditional understanding of neutrophils as simple first-line defenders against infection. "These results challenge the traditional view of neutrophils as simple first-line defenders," says Magdalini Lourda, senior author of the study and senior research specialist at the Department of Laboratory Medicine. "They appear to have a wider role in shaping immune responses, which may be important when designing future treatments." Why Does Strep Throat Lead to Autoimmune Problems? Strep throat affects approximately 5.2 million people in the United States each year, and for most, antibiotics clear the infection completely. However, in a small percentage of cases, as many as 1 in 200 children diagnosed with certain post-streptococcal autoimmune conditions, the infection can leave lasting effects on the immune system. Scientists have identified two main mechanisms that explain how strep can trigger autoimmune disease. The first is molecular mimicry, which occurs when components of the strep bacteria closely resemble the body's own proteins, tricking the immune system into attacking both the invader and the body's own cells. The second mechanism involves an unusually large, non-specific immune response, where the Group A Streptococcus bacterium releases a "super" antigen that causes such a broad inflammatory response it attacks healthy tissue along with the bacteria. How to Protect Yourself and Recognize Warning Signs - Seek prompt treatment: If you experience severe sore throat, fever, and swollen tonsils, see a healthcare provider for testing. Strep throat is diagnosed with a rapid test or throat culture, and early antibiotic treatment can prevent complications. - Complete your full antibiotic course: Even if symptoms improve within a few days, finishing all prescribed antibiotics is critical to eliminate the infection completely and reduce the risk of post-streptococcal complications. - Watch for delayed symptoms: Be aware that autoimmune complications can appear weeks or even months after the sore throat resolves. These may include sudden skin inflammation, joint pain, heart problems, or neurological symptoms like tics or obsessive-compulsive behaviors. - Maintain good hygiene: Strep spreads through close contact with infected individuals. Wash hands regularly, avoid sharing drinks or utensils, and keep distance from people with active strep infections when possible. The research also reveals that post-streptococcal immune reactions may affect the brain. Immune cells activated by a strep infection may travel along the nerves connecting the nose to the brain and can weaken the blood-brain barrier, allowing immune cells and antibodies to enter brain tissue where they don't normally belong. This can amplify inflammation in the central nervous system and may explain why some children suddenly develop neurological symptoms following a strep infection. Beyond guttate psoriasis, strep throat has long been linked to other delayed complications affecting multiple body systems. These include rheumatic fever, which can damage the heart; PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections), often characterized by sudden onset of obsessive-compulsive behaviors or tics; and potentially chronic fatigue syndrome, a condition marked by extreme exhaustion lasting at least six months. The Karolinska Institutet research team plans to validate their findings in larger and more diverse patient groups, including people with plaque psoriasis, to determine whether antigen-presenting neutrophils can serve as predictive biomarkers or potential drug targets. They also aim to clarify which molecular signals cause neutrophils to change behavior and how they interact with T cells in early autoimmune inflammation. While strep throat remains one of the most common bacterial infections globally, affecting approximately 600 million people each year, understanding these immune mechanisms offers hope for better prevention and treatment strategies in the future.
