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HLA molecules, bacteria and autoimmunity
1Division of Life Sciences, Infection and Immunity Group, King's College, 150 Stamford Street, London and *Department of Rheumatology, UCL School of Medicine, Middlesex Hospital, London.
Journal of Medical Microbiology
|February 7, 2001
Summary
Human leukocyte antigen (HLA) associations, like HLA-B27 in ankylosing spondylitis and HLA-DR1/DR4 in rheumatoid arthritis, are linked to rheumatic diseases. This review explores the pathological roles of specific bacteria, such as Klebsiella pneumoniae and Proteus mirabilis, in these conditions.
Area of Science:
- Immunogenetics
- Rheumatology
- Microbiology
Background:
- Many diseases are linked to Human Leukocyte Antigen (HLA) genes.
- Specific HLA associations, particularly HLA-B27 in ankylosing spondylitis (AS) and HLA-DR1/DR4 in rheumatoid arthritis (RA), are well-established.
- Reactive arthritis (ReA) is triggered by infections like Chlamydia and gastrointestinal bacteria.
Purpose of the Study:
- To review the pathological implications of HLA associations in rheumatic inflammatory conditions.
- To explore the link between specific bacteria (Klebsiella pneumoniae, Proteus mirabilis) and HLA associations in AS and RA.
Main Methods:
- Review of existing microbiological and immunological studies.
- Analysis of established associations between HLA antigens and rheumatic diseases.
- Examination of bacterial triggers for reactive arthritis.
Main Results:
- 96% of AS patients possess HLA-B27, compared to 8% in the general population.
- >90% of RA patients possess HLA-DR1 or HLA-DR4 subtypes, versus 35% in the general population.
- Associations found between Klebsiella pneumoniae and AS, and Proteus mirabilis and RA.
Conclusions:
- The review highlights the potential pathological roles of specific bacteria in HLA-associated rheumatic diseases.
- Understanding these associations may offer insights into the pathogenesis of ankylosing spondylitis and rheumatoid arthritis.
- Further research into the interplay between HLA, microbial triggers, and disease development is warranted.