Possible Role of Molecular Mimicry in Lyme Arthritis
Year: 2003
Type: book-chapter
Abstract: Molecular mimicry has been raised as an important hypothesis to explain the onset of inappropriate responses to self-antigens in some autoimmune diseases. This mechanism is defined by the presence of shared amino acid (aa) regions between foreign and self-proteins. Examples of presumed mimicry have been reported for epitopes recognized by both T- and B-cells. In the mimicry model, the initiation of autoimmune symptoms is believed to be the result of the persistence of immune cells generated by the host in response to an infectious agent (see Fig. 1A). These cells then recognize similar or identical epitopes within host tissue (see Fig. IB). True molecular mimicry is marked by the cross-reactivity of a strong microbial antigen with a tissue-specific or ubiquitous host epitope. Once an immune response is generated, the persistence of the microbial antigen is not necessary for the maintenance of the immune response.
Source: Humana Press eBooks
Authors: Abbie L. Meyer, Brigitte T. Huber
Language: English
Subfield: Parasitology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W137715551