Related Experiment Videos
Epitope mimics and determinant spreading: pathways to autoimmunity.
A D Farris1, C L Keech, T P Gordon
1Department of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria, Australia.
Cellular and Molecular Life Sciences : CMLS
|December 29, 2000
Summary
Pathogens use molecular mimicry to evade detection. This review explores how T cell molecular mimicry may contribute to the development of systemic autoimmunity in mammals.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmunity
Background:
- Pathogens evolve to mimic host molecules for propagation.
- Mammalian immune systems develop diverse repertoires to combat pathogens.
- Immune repertoire diversity can lead to self-reactive lymphocytes.
Purpose of the Study:
- To review the role of molecular mimicry in the development of systemic autoimmunity.
- To explore the connection between T cell mimicry and autoimmune diseases.
Main Methods:
- Literature review of studies on molecular mimicry and autoimmunity.
- Analysis of T cell responses to pathogen- and self-antigens.
- Examination of regulatory mechanisms controlling self-reactivity.
Main Results:
- Molecular mimicry by infectious agents can trigger autoimmune responses.
- T cell cross-reactivity between pathogen and self-antigens is a key mechanism.
- Dysregulation of immune tolerance can lead to systemic autoimmunity.
Conclusions:
- Molecular mimicry at the T cell level is a significant factor in systemic autoimmunity.
- Understanding these mimicry mechanisms is crucial for developing autoimmune disease therapies.