Are there unique autoantigens triggering XXXX ?

@entity1252 @entity1737 @entity1723 @entity792 @entity934
Using three reference @entity1723 ( @entity1723 ) as a prototype of T-cell mediated organ-specific @entity792 , @entity1737 ( @entity1737 ) as a prototype of autoantibody-mediated organ-specific @entity792 and @entity1252 ( @entity1252 ) as a prototype of non-organ-specific @entity792 --we have reached several conclusions: 1) All three diseases are associated with the presence of multiple autoantibodies and/or autoreactive T cells that recognize a large number of antigenic molecules. The apparent predominant role of certain antibodies in some diseases could relate to their functional properties such as @entity934 receptor (AChR) blockade for anti-AChR autoantibodies in @entity1737 or anti-dsDNA in @entity1252 . 2) Major target antigens are clustered in the target cell affected by organ-specific @entity792 : beta cells in @entity1723 , striated-muscle cells in @entity1737 , or apoptotic cells in the case of @entity1252 . 3) Antibodies and T cells recognize multiple epitopes in these molecules. 4) The most evident explanation for the observed clustering and diversity is autoantigen spreading. Spreading probably involves T cells secreting proinflammatory cytokines but also possibly antibodies as in the case of nucleosome autoantibodies in @entity1252 . 5) The counterpart of antigen spreading is bystander suppression in which regulatory cytokines deviate the immune response towards a protective response. 6) The mechanisms underlying the initiation of the autoimmune response and antigen spreading are still undetermined. They could imply a direct abnormality of the target cell in the case of organ-specific @entity792 (e.g. infection with a virus showing a selective tropism for the target cell in organ-specific @entity792 , or loss of physiological regulation of major histocompatibility complex molecule expression) or could be consequence of a ubiquitous cell abnormality such as increased apoptosis in @entity1252 . The respective roles of genetic and environmental factors in these triggering events remain to be determined.
