Autoimmunity is characterized as a state of abnormal specific humoral and cell-mediated responses against constituents of body tissues. One time- honored approach to explaining the pathogenesis of autoimmunity has been application of the Koch's postulates, on loan from the field of microbiology suggesting that autoantibodies and/or autoreactive T cells are the presumed 'pathogens' of autoimmunity, and that passive transfer of these autoimmune factors to susceptible animals will result in the induction of the autoimmune disease. We suggest that autoimmunity is not in many cases due to the presence of factors leading to the autoimmune response in those susceptible. Instead, it is the lack of a factor which leads to the development of autoimmunity, a factor (cytokine, protein, gene, etc.) which is present in the healthy individual and normally protects in from disordered immune regulation. We propose to direct more research into therapeutic modulation of autoimmunity by administration of putative 'protective factors', rather than by attempts to depress or remove autoreactive cells and antibodies from the autoimmune.
|Original language||English (US)|
|Number of pages||8|
|Journal||Archivum Immunologiae et Therapiae Experimentalis|
|State||Published - Mar 13 1999|
- Autoreactive cells
ASJC Scopus subject areas
- Immunology and Allergy