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S-antigen: from gene to autoimmune uveitis.
T Shinohara1, V K Singh, M Tsuda
1Molecular Biology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
Experimental Eye Research
|June 1, 1990
Summary
Retinal S-antigen (S-Ag) triggers experimental autoimmune uveitis (EAU). This study reveals antigenic mimicry between self and non-self proteins, offering insights into autoimmune inflammation mechanisms.
Area of Science:
- Immunology
- Ophthalmology
- Molecular Biology
Background:
- Retinal S-antigen (S-Ag) induces experimental autoimmune uveitis (EAU), a model for human uveitis.
- Understanding the molecular basis of EAU is crucial for developing treatments for autoimmune eye diseases.
Purpose of the Study:
- To determine the nucleotide and amino acid sequences of the S-Ag gene and its cDNAs.
- To identify uveitopathogenic sites within S-Ag and investigate their homology with non-self proteins.
- To explore the role of antigenic mimicry in the induction of EAU.
Main Methods:
- Nucleotide sequencing of S-Ag gene and cDNAs.
- Amino acid sequence deduction and comparison with microbial and viral proteins.
- Immunization of Lewis rats with S-Ag peptides and yeast histone H3.
- Assessment of EAU induction and T-cell proliferation assays.
Main Results:
- Identified four uveitopathogenic sites in bovine S-Ag, with one site (peptide M) showing homology to various non-self proteins.
- Mononuclear cells from peptide M-immunized animals proliferated in response to synthetic peptides from foreign proteins.
- Synthetic peptides and native yeast histone H3 induced EAU in Lewis rats, demonstrating dose-dependent effects.
Conclusions:
- Established evidence of antigenic mimicry between self (S-Ag) and non-self proteins.
- These findings provide a foundation for further research into the mechanisms of autoimmune inflammation in uveitis.