Key result
The progression from benign autoimmunity to pathogenic autoimmune disease following infection depends upon the balance of cytokines produced during the inflammatory process.
Understanding cytokine profiles during infection may offer a promising approach to preventing post-infection autoimmune responses.
May guide cytokine profiling to flag post-infection autoimmune risk; leaves open prospective validation before clinical adoption.
Autoimmune disease has long been considered a shadow following infectious diseases. Epidemiological evidence shows that rheumatic fever follows streptococcal infection and Trypanosoma cruzi infection is the instigator of Chagas' disease. There is, however, very little information of the mechanism by which such a train of events is initiated. Autoimmunity, in a form of autoantibodies, is common after many infections and may well result from the mimicking of host proteins by antigens of the infectious agent. There are, however, few if any examples in humans where molecular mimicry gives rise to autoimmune disease. The progression from benign autoimmunity to pathogenic autoimmune disease depends upon the balance of cytokines produced during the inflammatory process accompanying infection. In many autoimmune diseases, the cytokine profile favors the proinflammatory cytokines, IFN-gamma and IL-1, which support the production of disease. A searching study of cytokine profiles during infection may offer a promising approach to avoiding the harmful consequences of post-infection autoimmune responses.
No takes yet. Share an insight, caveat, or question.
Noel R. Rose (1998) conducted a review in Autoimmune disease. The progression from benign autoimmunity to pathogenic autoimmune disease following infection depends upon the balance of cytokines produced during the inflammatory process.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: