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HLA-B27 binding of peptide from its own sequence and similar peptides from bacteria: implications for
R H Scofield1, B Kurien, T Gross
1Arthritis and Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA.
Abstract:
The spondyloarthropathies are associated by an unknown mechanism with HLA-B27 and certain bacteria. HLA-B27 shares sequence with proteins from enteric bacteria. The B*2705 sequence contains a nonapeptide, LRRYLENGK, predicted to bind in the binding cleft of B27. Some nonapeptides from enteric organisms that share sequence with this nonapeptide of B27 also bind B27. These observations suggest an unappreciated mechanism for autoimmunity that may operate in the B27-associated spondyloarthropathies involving peptides bound to and derived from histocompatibility alleles.
Insights
Human leukocyte antigen B27 (HLA-B27) may trigger autoimmune diseases like spondyloarthropathies through molecular mimicry. Bacterial peptides sharing sequences with HLA-B27 could initiate this autoimmune response.
Area of Science:
- Immunology
- Genetics
- Microbiology
Background:
- Spondyloarthropathies are linked to HLA-B27 through unknown mechanisms.
- HLA-B27 shares sequence similarities with proteins found in enteric bacteria.
Purpose of the Study:
- To investigate the potential mechanism of autoimmunity in HLA-B27-associated spondyloarthropathies.
- To explore the role of molecular mimicry between bacterial peptides and HLA-B27.
Main Methods:
- Sequence analysis of HLA-B27 and bacterial proteins.
- Prediction of peptide binding to the HLA-B27 binding cleft.
Main Results:
- A specific nonapeptide (LRRYLENGK) within HLA-B*2705 was identified as potentially binding to B27.
- Enteric bacterial nonapeptides with sequence homology to the B27 nonapeptide also demonstrated binding to B27.
Conclusions:
- Molecular mimicry involving bacterial peptides may be an unappreciated mechanism in B27-associated spondyloarthropathies.
- Peptides bound to and derived from histocompatibility alleles could play a role in initiating autoimmunity.