https://www.selleckchem.com/products/way-262611.html Anti-cytokine autoantibodies (AAbs) associated with an infectious phenotype are now included along with anti-complement AAbs and somatic pathogenic gene variants as a distinct category termed 'phenocopies of primary immunodeficiencies' in the classification of inborn errors of immunity. Anti-cytokine AAbs target specific cytokine pathways, leading to inordinate susceptibility to specific organisms, generally in the setting of immunocompetence. Anti-cytokine AAbs are detected in the majority of healthy individuals and may play a regulatory role in limiting exaggerated responses to cytokines. While it is not well understood why some individuals with anti-cytokine AAbs develop increased susceptibility to organisms of low pathogenicity and others do not, it is likely that genetics and environment play a role. To date, AAbs to interferon gamma (IFNγ), interferon alpha (IFNα), interleukins-17 and 22 (IL-17/IL-22), interleukin-6 and granulocyte macrophage colony stimulating factor (GM-CSF) and their association inating area of research. Evaluating generally immunocompetent individuals who present with chronic, treatment refractory, or unusual infections for anti-cytokine AAbs is critical as it may direct therapy and disease management. Autoimmune endocrine diseases can be thought of as a case of mistaken identity. The immune system mistakenly attacks one's own cells, as if they were foreign, which typically results in endocrine gland hypofunction and inadequate hormone production. Type 1 diabetes mellitus and autoimmune thyroid disorders (Hashimoto and Graves diseases) are the most common autoimmune endocrine disorders, while conditions such as Addison disease are encountered less frequently. Autoantibody production can precede clinical presentation, and their measurement may aid verification of an autoimmune process and guide appropriate treatment modalities. In this review, we discuss type 1 diabetes mellitus, autoimmu