Autoimmune Disorders on the Rise: Pathways to Understanding and Prevention

Abstract Autoimmune disorders occur when the immune system mistakenly attacks the body’s self-tissues due to a breakdown in tolerance mechanisms that prevent self-reactivity. Autoimmune diseases disproportionately impact females, who represent approximately 78% of autoimmune patients. The increasing prevalence of autoimmunity, as evidenced by rising antinuclear antibody (ANA) biomarkers, is concerning. Between 2011-2022, approximately 15 million people in the U.S. were diagnosed with autoimmune disorders, with 34% having more than one autoimmune disease. Key mechanisms contributing to autoimmunity include abnormalities in thymic selection, where autoreactive T cells escape deletion, and failure of regulatory T cells (Tregs) to suppress harmful immune responses. Environmental factors, such as viral infections or chemical exposures, may alter self-antigens, causing the immune system to misidentify them as foreign through molecular mimicry. In rare cases, anatomically sequestered antigens, normally hidden from immune surveillance, are released, leading to autoimmunity. Inappropriate expression of major histocompatibility complex (MHC) molecules on non-antigen-presenting cells can aggravate autoimmune conditions. Additionally, the interplay of genetics, hormones, and gut microbiota may play a role in causing autoimmune conditions. Autoimmune diseases may not be entirely preventable. However, strategies such as healthy diet, stress management, exercise, toxin avoidance, gut health support, and routine health check-ups can reduce risk or delay onset. This review explores the factors driving the rise of autoimmune disorders, their prevalence, the mechanisms behind their development, and preventive measures to reduce the risk or delay autoimmune onset. Understanding these mechanisms may lead to improved treatments, given the significant impact of autoimmunity on global health. Keywords: Autoimmune disorders, ANA, thymic selection, Tregs, molecular mimicry, autoimmunity, MHC.