The immune response in autoimmune disease recapitulates that of responses directed against infection, except that self antigens are, or become, the target of the adaptive immune system. These self antigens may drive a process that is localised within a specific organ, such as the thyroid gland (Grave’s disease, Hashimoto’s thyroiditis) or brain (multiple sclerosis). Or responses to them may lead to a more general inflammatory condition (e.g. systemic lupus erythematosus [SLE]). Following initiation and trafficking, local damage can amplify disease, while the balance of this by regulation determines whether relapse or remission dominate as the disease progresses.Autoimmune disease occurs when an immune response attacks our own tissues. Like all adaptive immune responses, it is focused on specific antigens by T-cell receptors and B-cell receptors. In contrast to infection, the antigens that these cells recognise are processed from proteins within the target organ and this drives a chronic inflammatory process that disrupts the normal function of the tissue.In human diseases the trigger for this process cannot usually be determined. There is evidence that autoimmunity can follow infection, but that more than one infection can initiate disease. Other environmental factors are also relevant but are not well defined.