Autoimmunity and infection in Sjögren's syndrome.

PURPOSE OF REVIEW

To summarize the recent developments concerning the potential viral pathomechanisms and involvement of viruses in Sjögren's syndrome, and to highlight the areas for future research and therapies.

RECENT FINDINGS

Activated IFN-1 pathway plays an important part in the autoimmune disease process of Sjögren's syndrome; therefore, several therapies aiming to reduce or inhibit the IFN-1 production and its effects may be a target for future treatment plans. Activated aryl hydrocarbon receptor may interact with latent Epstein-Barr virus (EBV) infection, which in turn may predispose to the development of Sjögren's syndrome. It is estimated that the population is 95% positive for EBV serology. Microbial factors may incite autoimmune disease. Although this hypothesis is proven in a few illnesses such as rheumatic fever, there is no definitive evidence of an infectious environmental trigger in Sjögren's syndrome. However, there are circumstantial data with regard to viruses and several potential mechanisms of disease. These include antigen mimicry, polyclonal lymphocyte activation, and infection-mediated innate end-organ inflammation. In addition, hepatitis C virus infection clearly causes a Sjögren's-syndrome-like illness.

SUMMARY

Data continue to implicate viral infection in the cause of Sjögren's syndrome, but there are no definitive studies incriminating a particular virus.