The relationship between infection and autoimmunity has been increasingly defined over the last twenty years or so. It is now quite clear that, in genetically susceptible individuals, environmental factors (mainly infections) play a critical role in the pathogenesis of autoimmune diseases. It is believed that infections contribute to the maturation of the immune system from the innate to adoptive phases, and that bacterialand viral infections are arthritogenic stimulants leading to various rheumatic conditions. A failure to isolate these microorganisms is probably due to the action of the immune system, but often casts doubt on their role in the pathogenesis of autoimmune diseases. Among bacteria, Helicobacter pylori has been associated with diseases such as autoimmune gastritis, Sjögren’s syndrome, atherosclerosis, immune thrombocytopenia purpura, inflammatory bowel diseases and autoimmune pancreatitis, in each of which it seems to play a pathogenatic, but it has also been suggested that it may help to protect against the development of autoimmune gastritis, multiple sclerosis, systemic lupus erythemathosus and inflammatory bowel diseases. Infectious agents may play a dual role in the etiopathogenesis of antiphospholipid syndrome (APS): they may be the initial trigger of the production of antibodies cross-reacting with beta 2 glycoprotein I (β2GPI) and infectious peptides, and β also induce an inflammatory response. According to the two-hit theory, pathogenetic anti-β2GPI antibodies act as β the first hit whereas inflammatory responses may represent the second hit The slowly growing Propionibacterium acnes may be involved in the etiopathogenesis of SAPHO syndrome by triggering the non-specific activation of cellmediated immunity. Its ability to persist in bone lesions in a form that is incompatible with culturing suggests the possibility an arthritis that is secondary to a “persistent” infection.