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Autoimmune disease and molecular mimicry: an hypothesis
1Hepato-biliary and Liver Transplantation Unit, Royal Free Hospital, Hampstead, London, UK.
Trends in Biochemical Sciences
|April 1, 1993
Summary
Molecular mimicry may explain autoimmune diseases. Microbial peptides presented by antigen-presenting cells can trigger helper T cells to attack self-tissues expressing similar peptides inappropriately.
Area of Science:
- Immunology
- Molecular Biology
- Pathogenesis
Background:
- Helper T lymphocytes initiate immune responses via Class II Major Histocompatibility Complex (MHC) molecule recognition.
- Antigen-presenting cells constitutively express Class II MHC molecules, crucial for initiating immune responses.
- Aberrant Class II MHC expression on non-professional cells occurs in disease states.
Purpose of the Study:
- To propose a hypothesis for autoimmune disease pathogenesis.
- To explore the role of molecular mimicry in autoimmune reactions.
Main Methods:
- Hypothetical model based on molecular mimicry.
- Analysis of peptide presentation by Major Histocompatibility Complex molecules.
Main Results:
- Molecular mimicry between microbial/viral peptides and self-peptides is proposed.
- Inappropriate presentation of self-peptides on target tissues can occur.
Conclusions:
- Infectious agent-derived peptides can stimulate helper T cells.
- This stimulation can lead to an autoimmune attack on self-tissues via molecular mimicry.