Autoantibodies in myositis.

Several autoantibodies are found specifically in myositis. Mostly this is myositis in the context of a connective tissue disease with associated features such as Raynaud's phenomenon, arthralgias, pulmonary fibrosis or scleroderma. The patterns of disease amount to overlap syndromes or subsets in which one can often predict the presence of a particular type of autoantibody. There are HLA associations, particularly with DQ alleles, related more closely to the antibody than to myositis overall. There is also a suggestion of seasonal and geographical variation within the United States distinguishing the advent of particular autoantibodies with the myositis. The myositis antigens are mainly ribonucleoprotein particles (RNA-protein complexes) functioning in RNA processing, protein translation and protein translocation into the endoplasmic reticulum. Within the cell the antigens are not accessible to antibody, with the possible exception that antibody to U(1)RNP may enter cells. If antibodies are to have a role in pathogenesis it is more likely to be through binding to cell membranes (there to activate complement or mediate T lymphocyte activity) or through immune complex mechanisms. The myositis antigen Ku has been detected on cell membranes, but generally in myositis there is scant deposition of immunoglobulin or complement in muscle except within small blood vessels. If autoantibodies really have little part to play in the pathogenesis of myositis their existence must relate to the earlier events of aetiology, like fingerprints on fragments of a terrorist's bomb.