Autoimmunity Reviews 3 (2004) 10–15
1568-9972/04/$ - see front matter ᮊ 2003 Elsevier Science B.V. All rights reserved.
Disease mimicry—a pathogenetic concept for T cell-mediated
autoimmune disorders triggered by molecular mimicry?
Jorg Christoph Prinz*
Department of Dermatology, Ludwig-Maximilians-University, Frauenlobstr. 9-11, Munich 80337, Germany
Received 6 November 2002; accepted 28 April2003
Molecular mimicry is considered as a mechanism by which infectious pathogens may break immunological
tolerance and cause autoimmune disease. It implicates that peptides shared between pathogen and host may induce
cross-reactive immune reactions. According to this hypothesis, the resulting autoimmune response actually
represents a secondary immune response. It is mediated by cross-reactive T cells that have been educated in a
primary immune response against a particular pathogen. Using psoriasis vulgaris as a model, this article discusses
the potential functional consequences molecular mimicry should have for the resulting autoimmune disease. It
proposes that due to the functional memory of T cells, which is an integral feature of adaptive immunity, the
phenotype of an autoimmune disease induced by molecular mimicry should reflect the immune mechanisms raised
in the primary immune response. This process might be called ‘disease mimicry’.
ᮊ 2003 Elsevier Science B.V. All rights reserved.
Keywords: Molecular mimicry; Disease mimicry; Psoriasis; Bacterial trigger; Autoimmunity
The development of many T cell-mediated auto-
immune disorders has been etiologically linked to
infectious agents. A modelproposed to account
for this link is molecular mimicry
. It suggests
that pathogen expresses a stretch of protein that
shares antigenic structures with host tissue. If this
pathogen-encoded epitope is presented by the
major histocompatibility complex, it may activate
potentially self-reactive T cells. As a consequence,
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muenchen.de (J.C. Prinz).
the tolerance to autoantigens breaks down and the
pathogen-specific immune response cross-reacts
with host structures to cause tissue damage and
This model provides a highly attractive expla-
nation of how infection breaks tolerance, and it
has been linked to the pathogenesis of several
. Molecular mimicry,
however, bears another intriguing aspect that so
far has not received attention. In addition to
providing the trigger for autoimmunity, it should
crucially affect the particular type of the subse-
quent autoimmune tissue reaction. The reason for
this is that an autoimmune response resulting from
molecular mimicry actually represents a secondary