A number of patterns of illness affecting joints or muscles are associated with antibodies to "self" molecules and are, therefore, called autoimmune rheumatic diseases. They include rheumatoid arthritis, systemic lupus erythematosus, anti-phospholipid syndrome, polymyalgia rheumatica, systemic slcerosis, Sjögren’s syndrome, polymyositis and dermatomyositis, necrotising arteritis, myasthenia gravis, sarcoidosis, and a spectrum of related syndromes. Rheumatological features also occur with autoimmune thyroid disease.

Although the mechanisms of these disorders are not fully understood it seems increasingly likely that they share two common elements. Firstly, the clinical features are directly due to the autoantibodies. This was in doubt for many years but clarification of the pathways involved indicates that it is almost always the case. Secondly, the autoantibodies perpetuate their own production through various means.

It has often been assumed that autoimmune disease is like rheumatic fever - due to an immune response to some "trigger" infection leading to a cross reactive response to self molecules. However, there is no evidence for this. The timing of onset of autoimmunity is random. This is most easily explained by the fact that individual antibodies are created at random. Self antigens are always available, so autoantibodies whose production is permitted will appear in the blood soon after t hey are first created and persist life long - as is observed. The reasons why production of certain specific types of autoantibody is permitted are complex. It is likely that these autoantibodies stimulate their own production by bypassing or reversing control mechanisms. In a sense, autoantibody-associated disease is truly "idiopathic"; it causes itself.