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Molecular mimicry between non-self, modified self and self in autoimmunity

A E Karlsen¹, T Dyrberg

¹Steno Diabetes Center, Gentofte, Denmark.

Seminars in Immunology

|April 8, 1998

Summary

Molecular mimicry, where foreign and self antigens share epitopes, rarely causes autoimmune disease due to immune regulation. However, it is linked to various autoimmune conditions, highlighting its complex role.

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Area of Science:

Immunology
Autoimmunity
Molecular Biology

Background:

Molecular mimicry involves shared epitopes between foreign and self-antigens at B and T cell levels.
The immune system typically prevents harmful self-reactivity, despite molecular mimicry.
Various autoimmune diseases are associated with molecular mimicry, indicating a complex interplay.

Purpose of the Study:

To review the concept of molecular mimicry.
To discuss its relevance in initiating autoimmune diseases.
To explore mimicry between foreign-self and self-modified self-epitopes.

Main Methods:

Literature review and conceptual analysis.
Discussion of immune regulatory mechanisms.
Examination of epitope sharing in autoimmunity.

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Main Results:

Molecular mimicry is a common immunological phenomenon.
Effective immune regulation usually prevents autoimmune responses.
Despite regulation, molecular mimicry contributes to autoimmune disease initiation.

Conclusions:

Molecular mimicry is a significant factor in autoimmune disease pathogenesis.
Understanding molecular mimicry is crucial for autoimmune disease research.
The balance between immune tolerance and molecular mimicry dictates autoimmune outcomes.