Autoimmune diseases define a group of disorders characterized by the immune system's inability to distinguish between self and non-self-antigens, leading to immunological attack of the body's own tissues. Understanding autoimmune diseases involves exploring the mechanisms underlying self-tolerance breakdown, understanding immune activation against self-antigens, and determining how these processes result in tissue damage. Autoimmune diseases often arise due to the breakdown of self-tolerance mechanisms that normally prevent the immune system from attacking its own tissues. Central tolerance, established in the thymus and bone marrow, involves eliminating self-reactive T cells and B cells. Peripheral tolerance mechanisms, including regulatory T cells (Tregs) and anergy (lack of T cell responsiveness), further prevent the activation of self-reactive immune cells. In some cases, infectious agents may share molecular structures with self-antigens. This can lead to a phenomenon called molecular mimicry, where the immune response against the pathogen cross-reacts with self-antigens, triggering autoimmunity. In autoimmune diseases, B cells may produce autoantibodies that target self-antigens. These autoantibodies can contribute to tissue damage through various mechanisms, including complement activation, immune complex deposition, and direct cell destruction. Autoreactive T cells that escape thymic deletion or peripheral tolerance mechanisms can recognize and attack self-antigens. CD4+ T helper cells, particularly Th1 and Th17 subsets, are often implicated in autoimmune diseases, as they secrete pro-inflammatory cytokines that drive tissue inflammation and damage. Imbalances in cytokine production can also play a role in autoimmune diseases. For example, pro-inflammatory cytokines, such as interleukin-17 (IL-17), can contribute to tissue inflammation. Genetic factors, particularly the human leukocyte antigen (HLA) genes, are known to contribute to susceptibility to autoimmune diseases. Certain HLA alleles may present self-antigens more effectively to immune cells, increasing the risk of autoimmunity. For example, in the context of rheumatoid arthritis, specific HLA-DRB1 alleles are strongly associated with the disease, whilst in celiac disease (gluten intolerance), HLA-DQ2 and HLA-DQ8 alleles are associated with disease susceptibility. Autoimmune diseases can be tissue-specific, targeting organs or tissues (e.g., Hashimoto's thyroiditis), or systemic, affecting multiple organs (e.g., systemic lupus erythematosus). The mechanisms and specific autoantigens can therefore vary widely between different diseases. Additionally, the immune response in autoimmunity can broaden to target additional self-antigens over time (termed epitope spreading), worsening the disease. Dysfunctional regulatory T cells (Tregs) or impaired immune regulatory mechanisms may also contribute to the development of autoimmune diseases by allowing autoreactive immune responses to persist. Environmental factors, such as infections, hormonal changes, and certain drugs, can also trigger or exacerbate autoimmune diseases by promoting immune dysregulation. Treatment of autoimmune diseases often involves immunosuppressive drugs, which aim to suppress the immune response and reduce inflammation. However, newer targeted therapies aim to modulate specific immune pathways whilst minimizing global immunosuppression. Each autoimmune disease has its unique pathogenesis, antigen targets, and clinical presentation. For example, multiple sclerosis involves the immune attack on myelin in the central nervous system, while Type 1 diabetes targets insulin-producing cells in the pancreas. We provide a wide product range of research reagents for studying autoimmune diseases, including PD-L1 antibodies, CTLA4 antibodies, IgG2a antibodies, CXCL11 ELISA Kits, and Glucose 6 phosphate isomerase ELISA Kits. Explore our full autoimmune diseases product range below and discover more, for less.