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Molecular mimicry: a mechanism for autoimmune injury
1Department of Neurology, University of Utah, Salt Lake City 84132.
Abstract:
Many mechanisms may account for immune-mediated pathology after viral infections. Although several means have been hypothesized to play a role in disease, a widely accepted mechanism for viral-induced autoimmunity is molecular mimicry. It is thought that damage could result from an immune response to similar regions shared between virus and the host. Using computer-aided analysis, many sequence homologies have been identified between virus and host antigens. Using peptides corresponding to these regions, immunologic cross-reactivity has been found. In some cases, monoclonal antibodies to peptides of these regions have been shown to directly induce or augment disease in animal models. Using this approach to identify similar regions, it is possible to associate a known autoantigen with an infectious agent in autoimmune diseases in which there is no known etiologic agent. Conversely, it would also be possible to associate a known viral constituent with an unknown host antigen. Furthermore, identification of disease-inducing regions of autoantigens or viral proteins may lead to immunotherapeutic approaches to establish tolerance or anergy to such disease-inducing regions.
Insights
Molecular mimicry, where viral and host similarities trigger autoimmune responses, is a key mechanism in post-viral pathology. Identifying these shared sequences aids in understanding and potentially treating autoimmune diseases.
Area of Science:
- Immunology
- Virology
- Autoimmunity
Background:
- Viral infections can trigger immune-mediated diseases.
- Molecular mimicry is a hypothesized mechanism for viral-induced autoimmunity, involving immune responses to shared viral and host sequences.
- Identifying these shared sequences is crucial for understanding disease etiology.
Purpose of the Study:
- To explore the role of molecular mimicry in viral-induced autoimmunity.
- To investigate the use of computer-aided analysis for identifying shared viral and host antigen sequences.
- To assess the potential for developing immunotherapies targeting disease-inducing regions.
Main Methods:
- Computer-aided sequence homology analysis to identify shared regions between viral and host antigens.
- Peptide synthesis corresponding to identified homologous regions.
- Immunological cross-reactivity assays using synthesized peptides.
- In vivo studies using monoclonal antibodies to assess disease induction or augmentation in animal models.
Main Results:
- Numerous sequence homologies between viral and host antigens were identified.
- Immunologic cross-reactivity was demonstrated using peptides from these homologous regions.
- Monoclonal antibodies targeting these regions could induce or augment disease in animal models.
Conclusions:
- Molecular mimicry provides a plausible mechanism for viral-induced autoimmunity.
- This approach can link specific infectious agents to autoantigens in autoimmune diseases.
- Identifying disease-inducing regions offers potential for novel immunotherapeutic strategies.