Infection, mimics, and autoimmune disease

The observation that infection can precipitate an autoimmune disease dates back more than a century. The first human autoimmune disease described, paroxysmal cold hemoglobulinuria, was thought of as a late consequence of syphilis, and rheumatic fever is still associated with preceding streptococcal infection. In modern times, these associations have been attributed to molecular mimicry. In its simplest form, the concept of molecular mimicry states that antigenic determinants of infectious microorganisms resemble structures in the tissues of the host but differ enough to be recognized as foreign by the host's immune system. It is now clear that mimicry on the molecular level is a common phenomenon; that is, many sequential and structural determinants of infectious agents simulate epitopes of host tissues (1). But, as Mackay and I remarked recently, "There are, as yet, no firm instances of molecular mimicry by microorganisms serving as initiating agents of human autoimmune disease" (2).