Autoimmunity and Triggers
March 4, 2024 | Rheumatic Disease
What does “autoimmune” mean anyway?
Think of it this way: the immune system acts as an army of cells whose purpose is to protect the body (“self”) against foreign invaders (“non-self”) like bacteria, viruses, and abnormal cells like cancer cells. Thus, it is important that the immune system recognizes “self” from “non-self.”
In individuals with an autoimmune disease, the immune system recognizes itself as foreign and inappropriately activates the immune system, sending immune cells to attack various parts of the body, resulting in organ damage. Depending on the target organ involved, like skin, joints, pancreas, or the brain; you can have rheumatoid arthritis, systemic lupus erythematosus (SLE), Hashimoto’s thyroiditis, type 1 diabetes, multiple sclerosis, psoriasis, or one of the many more possible autoimmune diseases.
Why does the immune system break down? What are some factors that have been associated with the onset of autoimmune disease?
These are difficult questions to answer, as association does not mean causation.
First, we know that genetics play a role. Some people who have an autoimmune disease have a certain genetic tendency that increases their risk. For example, it has been shown that the immune system gene HLA-DR4 is associated with a higher risk of developing rheumatoid arthritis (RA). In other words, having this gene increases your chances of developing RA, but does not guarantee that the person will develop RA.
In identical twins with the same genetic makeup, it’s been observed that one twin may develop an autoimmune disease, while the other person does not. It’s clear that there are factors, beyond a person’s genetic makeup, that contribute to a person’s chance of developing an autoimmune disease.
What are some environmental factors that may trigger an autoimmune disease?
Some infections may increase the chance of developing an autoimmune disease. One virus in particular - Epstein Bar virus (EBV) – has been studied across various autoimmune diseases, including SLE, Sjögren’s, and multiple sclerosis. This virus is highly prevalent and is known to cause mononucleosis in young adults. However, some people don’t even know they have been infected.
It is also believed that tobacco triggers an inflammatory response in the body. Smoking has been linked to the development of RA in genetically vulnerable people.
Medications have also been implicated in the development of autoimmune disease. Two medications for the heart and blood pressure - procainamide and hydralazine – have been shown in some studies to interfere with immune cell function and may be responsible for symptoms seen in drug-induced lupus. Fortunately, most drug-induced autoimmune diseases are reversible if the medicine is stopped.
Again, it is important to understand that while genetics, infections, smoking, and certain medications are associated with risk, none have been definitively shown to cause autoimmune disease. Instead, autoimmune disease is likely the result of complex interactions between both genetic and environmental risk factors.
Treating Your Autoimmune Disease
Regardless of what causes your autoimmune disease to develop, it is important that you receive proper care to manage your symptoms. The American College of Rheumatology encourages you to meet with your care team regularly to ensure you manage your disease and continue to live a healthy life.
About the Author
Kristen Lee, MD
Kristen Lee, MD, is the Rheumatology Team lead in Medical Affairs, North America at Pfizer. She trained at NYU School of Medicine and was Assistant Professor there before she joined industry. At NYU, she saw a diverse group of patients with complicated autoimmune diseases and contributed to the education of fellows and faculty. She is also a fellow of the American College of Rheumatology (ACR) and served on the Communications and Marketing Committee for the ACR. Dr. Lee’s interests include the pathogenesis of inflammatory arthritis and novel therapies for the treatment of autoimmune diseases. She is committed to the education of patients, fellows, and the rheumatology community. She lives in New York City.