Autor(es): Ang C Wim,Jacobs Bart C,Laman Jon D

Resumo: Molecular mimicry between microbial antigens and host tissue forms an attractive hypothetical mechanism for the triggering of autoimmune disease by preceding infections. Recent crucial reviews state that molecular mimicry, as the causative mechanism, remains unproven for any human autoimmune disease. However, the peripheral neuropathy Guillain-Barré syndrome (GBS) is largely overseen in this debate. Based on recent evidence, we argue that GBS should be considered as an excellent paradigm and an attractive model for elucidation of both host and microbial aspects of molecular mimicry.

Imprenta: Trends in Immunology, v. 25, n. 2, p. 61-66, 2004

Identificador do Objeto Digital: 10.1016/j.it.2003.12.004

Descritores: Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies ; Guillain-Barre Syndrome - Infectious diseases ; Guillain-Barre Syndrome - Immunology

Data de Publicação: 2004