These antibodies are found in a wide range of autoimmune diseases and in healthy controls (reviewed in Winfield and Jarjour, 1991). Anti-human chaperonin antibodies have been described in children with juvenile chronic arthritis, systemic lupus erythematosus, and cystic fibrosis (de Graeff-Meeder et al., 1993), in patients with Kawasaki disease (Yokota etal., 1993), and in patients with atherosclerosis (Xu et al., 1993), polymyositis, dermatomyositis, psoriatic arthritis, inflammatory bowel disease, epidermolysis bullosa aquisita, and bullous pemphigoid (Winfield and Jarjour, 1991). However, anti-human chaperonin autoantibodies were not found by other workers in the rheumatoid arthritis, Sjogren's syndrome, or Reiter's disease (Worthington et al., 1993; Winfield and Jarjour, 1991). In addition, there are numerous reports of anti-bacterial chaperonin antibodies in many autoimmune diseases (reviewed in Winfield and Jarjour, 1991; Kaufmann, 1994).
There is no evidence from animal models that antibodies to chaperonins induce autoimmune disease, and in any case chaperonin-specific antibodies are found in healthy individuals. Furthermore, in some autoimmune diseases there are conflicting reports regarding these antibodies. Anti-chaperonin antibodies do not seem to be directly involved in the pathogenesis of these autoimmune diseases, but provide useful indications of the extent of antichaperonin activation in autoimmune disease.
c. Chaperonins Detected in Autoimmune Lesions. Increased levels of cpn60 have been recorded in rheumatoid arthritis (Winrow et al., 1990; Karlsson-Parrs et al., 1990), juvenile chronic arthritis (Boog et al., 1992), atherosclerosis (Xu et al., 1993), multiple sclerosis (Selmaj et al., 1991), and ulcerative colitis (Winrow et al., 1994a). However, Sharif et al. (1992) could find only minor differences in the distribution of cpn60 in rheumatoid arthritis synovia, and so was unable to confirm increased expression of cpn60 in rheumatoid arthritis. Interestingly, these latter workers recorded that cpn60 is expressed in normal synovium. Other reports have shown that there is no increase in cpn60 expression in systemic lupus erythematosus patients (Dhillon et al., 1993) and those with Crohn's disease (Baca-Estrada et al., 1994). Is increased cpn60 expression associated with colocalization of T cells? In the chronic plaques of multiple sclerosis (Selmaj et al., 1991) and in chronic gastritis (Engstrand et al., 1991), cells that express chaperonins are colocalized with yd T cells. These data suggest that chaperonins are present in normal tissues as well as in diseased tissue, but there is conflicting evidence about upregulation of chaperonin expression in disease. What if the opposite happens; in other words, there is too little heat shock protein? Agsteribbe et al. (1993) has reported an association between reduced cpn60 in tissues (one-fifth of controls) and a fatal, systemic mitochondrial disease in a baby girl. This report suggests that insufficient cpn60 may have serious systemic consequences.
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