In a few cases we have evidence for a direct link between a specific infection and an autoimmune disease. The classical example is that of rheumatic fever following Streptococcal infection. Although in many cases the precise combination of pathogenetic mechanisms is not understood, there are three general types of mechanism which it is important to distinguish. We have already seen one example in Graves' disease where stimulatory antibodies dysregulate thyroid function. A counter effect can also be seen as in Myasthenia Gravis.
Rheumatic fever is an example of direct tissue pathology following antibody binding.
This term implies that the recognition of autoantigen by T cells leads to tissue destruction without requiring the production of autoantibody. In most cases we do not know what the relative contribution of these factors is, though mechanism 4 would have to be confined to those tissues which constitutively express the 'death' protein Fas or which express it as a consequence of inflammation. Systemic diseases such as SLE and vasculitis almost certainly result from autoantibody-antigen complexes and their consequences. Certain organs are especially sensitive to immune complex deposition particularly the kidney. SLE patients possess a wide variety of autoantibodies to both cytoplasmic and nuclear antigens.