Molecular Mimicry: Infection Inducing Autoimmune Disease

ISBN-13: 9783540255970 / Angielski / Twarda / 2005 / 180 str.

Michael B. A. Oldstone

Opis

The purpose of this review is to examine the potential role of molecular mimicry in the pathogenesis of human T-lymphotropic virus type 1 ((HTLV- 1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)). Comp- hensive reviews on the pathogenic mechanisms of HTLV-1-associated human diseases are available throughout the medical literature (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Osame 2002). Approximately 25 years ago the ?rst human retrovirus, HTLV-1, was isolated (Poeisz et al. 1980). Subsequently, infection with HTLV-1 was shown to cause adult T-cell leukemia (ATL) and HAM/TSP (Gessain et al. 1985; McFarlin and Blattner 1991; Osame et al. 1986; Poeisz et al. 1980; Yoshida et al. 1987). HTLV-1 may infect up to 30% of people in endemic areas and 10 20 million people worldwide (Barmak et al. 2003; Edlich et al. 2000). However, only 1% 5% develop either ATL or HAM/TSP, the remainder being clinically asymptomatic carriers of HTLV-1 (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Osame 2002). Why infection with HTLV-1 causes ATL or HAM/TSP in some people while the vast majority of individuals are asymptomatic is largely - known. Some possible factors that may differentiate the asymptomatic from the diseased state include viral strain, human histocompatibility leukocyte antigen (HLA), viral load, and the immune response (Bangham 2000, 2003; Barmak et al. 2003; Jacobson 2002; Levin and Jacobson 1997; Nagai and Osame 2003; Nagai et al. 1998; Niewiesk et al. 1994; Osame 2002)."

Spis treści

Molecular Mimicry, Microbial Infection and Autoimmune Disease: Evolution of the Concept.- A Virus-Induced Molecular Mimicry Model of Multiple Sclerosis.- Suppression of Autoimmunity via Microbial Mimics of Altered Peptide Ligands.- Molecular and Cellular Mechanisms, Pathogenesis and Treatment of Insulin-Dependent Diabetes Obtained Through Study of a Transgenic Model of Molecular Mimicry.- Trypanosoma cruzi-Induced Molecular Mimicry and Chagas’ Disease.- HTLV-1-Induced Molecular Mimicry in Neurologic Disease.- Molecular Mimicry: Anti-DNA Antibodies Bind Microbial and Non-Nucleic Acid Self Antigens.- The Structural Interactions Between T-Cell Receptors and MHC/Peptide Complexes Place Physical Limits on Self-Nonself Discrimination.- Subject Index