Allergies and autoimmune diseases are caused by the host's immune response imbalance to environmental substances or self antigens, leading to inflammation and tissue damage. For many years, allergies and autoimmune diseases have been regarded as completely opposite types of illnesses. Extracellular pathogens (allergens) promote the differentiation of CD4+cells into Th2 cells, leading to the release of interleukins IL-4, IL-5, and IL-13, which play a major pathogenic role in allergic diseases. On the contrary, intracellular pathogens play a crucial role in the pathogenesis of autoimmune diseases by inducing CD4+cells to differentiate into Th1 cells, producing interferon, tumor necrosis factor (TNF -β), and subsequently activating cytotoxic mechanisms such as macrophage activation and lysosomal acidification. Moreover, the specific cytokines produced by Th1 and Th2 cells have mutually inhibitory effects, providing support for the hypothesis that the two types of diseases may be mutually exclusive. However, in recent years, increasing evidence has shown the limitations of this theory. On the one hand, in addition to Th1 and Th2, research has discovered many new subsets of helper T cells, and it has been demonstrated that T cells can switch from one functional phenotype to another and redifferentiate. On the other hand, there are also examples of mixed immune responses in clinical practice.According to the standard pathophysiological paradigm, IgE mediates immediate allergic reactions, while other immunoglobulins are associated with autoimmunity. Specifically, IgE bound to allergens activates eosinophils/mast cells, causing an immediate hypersensitivity reaction that leads to the release of inflammatory mediators such as histamine and leukotrienes, as well as the recruitment of eosinophils at the site of stimulation in the later stages. IgG, IgM, and IgA are generally considered to be more associated with autoimmunity, triggering autoimmune responses through antigen neutralization, formation of immune complexes with complement activation, or activation of specialized phagocytic cells leading to cytotoxicity. However, new evidence is gradually eliminating the boundary between IgE and the binary of IgG, IgA, and IgM. IgG, IgA, and IgM may also cause non classical allergic reactions, and mast cells can pass through Fcγ RI and Fcγ RII binds to IgG or IgG immune complexes; IgG induced complement system activation can further promote non IgE mediated allergic reactions. On the contrary, IgE antibodies, especially autoantibodies, are involved in the pathogenesis of autoimmune diseases. For example, a large number of IgE autoantibodies (IgM anti IgE, IgG anti IgE) have been found in patients with systemic lupus erythematosus. For more information, please refer to the official account tweet "The role of IgE antibodies in autoimmune diseases".In recent decades, the incidence rate of allergic and autoimmune diseases has continued to increase. Research shows that both have common genetic determinants, common susceptibility sites, genetic pathways and genome regulatory sites, which suggests a common disease mechanism. Hygiene hypotheses, skin barrier damage, and changes in microbial populations are common risk factors for both types of diseases. Moreover, allergic diseases, such as atopic dermatitis, will increase the risk of some autoimmune diseases (rheumatoid arthritis, type 1 diabetes and alopecia areata); Early allergy is the main risk factor for developing autoimmune diseases in the future; Allergies and autoimmune diseases often coexist and occur early in patients with congenital immunodeficiency, which proves the correlation between allergies and autoimmune diseases.In terms of treatment, corticosteroids remain the main drugs for treating allergies and autoimmune diseases. Due to its anti-inflammatory and immunosuppressive effects, corticosteroids have shown good efficacy in both types of diseases, and their therapeutic effects depend on multiple molecular mechanisms, among which the most important is the inhibition of NF -κ The activity of B, NF-κ B is a key transcription factor involved in various molecules involved in the inflammatory response. And some newly developed drugs for treating allergic symptoms (such as biologics like omalizumab or small molecule drugs) may actually be effective in treating autoimmune diseases, and vice versa. In addition, from a cytological perspective, eosinophils, basophils, and mast cells not only play important roles in allergic diseases, but also participate in the pathogenesis of autoimmune diseases.Although increasing pathological and physiological evidence suggests a common pathogenesis between allergic and autoimmune diseases, clinical data is still limited to date. Among numerous autoimmune diseases, there is limited understanding of the unique characteristics of allergic patients, and the knowledge gap regarding the impact of autoimmunity on the progression of allergic diseases is far from being filled.In summary, allergies and autoimmunity are not two unrelated diseases, and they may work together to maintain acute or chronic immune-mediated tissue damage. This provides unprecedented opportunities for treatment, selectively or extensively targeting the core mechanisms of pan immune dysregulation, which is a promising strategy to tailor more precise treatment plans for patients with allergies and autoimmune diseases based on their specific needs.ReferenceClin Rev Allergy Immunol 2025; 68:13Nat Med 2024; 30:920Lancet 2023; 401:1878Adv Immunol 2019; 142:35