scholarly journals Absence of autoantibodies to peptides shared by HLA-B27.5 and Klebsiella pneumoniae nitrogenase in serum samples from HLA-B27 positive patients with ankylosing spondylitis and Reiter's syndrome.

1992 ◽  
Vol 51 (6) ◽  
pp. 783-789 ◽  
Author(s):  
D D de Vries ◽  
A J Dekker-Saeys ◽  
E Gyodi ◽  
U Bohm ◽  
P Ivanyi
Keyword(s):  
Ankylosing Spondylitis ◽  
Klebsiella Pneumoniae ◽  
Hla B27 ◽  
Reiter's Syndrome ◽  
Serum Samples ◽  
Reiter’S Syndrome

scholarly journals Autoantibodies to HLA B27 in the sera of HLA B27 patients with ankylosing spondylitis and Reiter's syndrome. Molecular mimicry with Klebsiella pneumoniae as potential mechanism of autoimmune disease.

1987 ◽  
Vol 166 (1) ◽  
pp. 173-181 ◽  
Author(s):  
P L Schwimmbeck ◽  
D T Yu ◽  
M B Oldstone
Keyword(s):  
Ankylosing Spondylitis ◽  
Klebsiella Pneumoniae ◽  
Biological Significance ◽  
Amino Acid Sequences ◽  
Peptide Sequence ◽  
Autoimmune Response ◽  
Computer Search ◽  
Hla B27 ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Ankylosing spondylitis (AS) and Reiter's syndrome (RS) both show a strong correlation with the HLA B27 haplotype. We studied whether sharing of homologous amino acid sequences in the HLA B27 antigen with an invading microbe might occur, and if so, what is the biological significance of such homology. In a computer search of the Dayhoff data bank, we found a homology of six consecutive amino acids between HLA B27.1 antigen residues 72-77 and Klebsiella pneumoniae nitrogenase residues 188-193. These shared sequences are hydrophilic, suggesting locations on molecules exposed to the cell surface. Immunochemical analysis showed that 18 of 34 sera from patients with RS (53%) and 7 of 24 sera from patients with AS (29%) contained antibodies that bound to a synthesized peptide sequence representing residues 69-84 of HLA B27.1. In contrast, only 1 of 22 sera from healthy, B27+ controls (5%) contained antibodies to this peptide (p less than 0.01). Sera from three HLA B27- patients with RS did not possess antibodies to the HLA B27 peptide. Additionally, greater than 40% of HLA B27 patients with AS or RS had antibodies to Klebsiella residues 184-193, while none of the normal nonarthritic HLA B27 haplotype subjects did. Our results suggest that an autoimmune response(s) directed against HLA B27.1 may be a pathogenic mechanism in a subset of patients with AS and RS. Further, this response may initially be induced against Klebsiella pneumoniae, a microorganism that shares sequence homology with HLA B27.

Arthritis and Foodborne Bacteria

1994 ◽  
Vol 57 (10) ◽  
pp. 935-941 ◽  
Author(s):  
JAMES L. SMITH
Keyword(s):  
T Cells ◽  
Ankylosing Spondylitis ◽  
Reactive Arthritis ◽  
Molecular Mimicry ◽  
Food Poisoning ◽  
Cell Subset ◽  
Bacterial Cells ◽  
Hla B27 ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Diarrheic episodes caused by the foodborne pathogens Campylobacter, Salmonella, Shigella or Yersinia may lead to a sterile arthritis such as reactive arthritis, Reiter's syndrome or ankylosing spondylitis. Reiter's syndrome and reactive arthritis have been shown to be sequelae in a few well-studied bacterial food poisoning outbreaks. Reactive arthritis, Reiter's syndrome and ankylosing spondylitis show strong familial association related to the gene for HLA-B27 (HLA = human leucocyte antigen) antigen. Why HLA-B27-positive individuals are more susceptible to arthritis is not known, but molecular mimicry between the HLA-B27 antigen and antigens of triggering bacteria has been demonstrated and this mimicry has been proposed as a mechanism involved in etiology of the arthritides. Antigens from bacteria that triggered the arthritis are present in arthritic joints but bacterial cells are not found. Antibodies and T-cells specific for the triggering bacteria have been demonstrated in arthritic patients. T-cells present in synovial joints respond specifically to the particular arthritic triggering pathogen. The cells that respond to bacterial antigens belong to the T-cell subset TH1 that secrete a limited number of cytokines but it is not known if cytokines are involved in arthritis. A few studies have demonstrated that T-cells from the joints of arthritic patients respond to both bacterial and human heat shock proteins indicating that autoimmunity may be involved in causation of arthritis. While only about 2% of a population exposed to a triggering infection will acquire arthritis, these individuals undergo pain and suffering as well as economic hardships as a result of their disease.

Presence of circulating immune complexes in Reiter's syndrome and ankylosing spondylitis

1981 ◽  
Vol 18 (2) ◽  
pp. 291-297 ◽  
Author(s):  
J.T. Rosenbaum ◽  
A.N. Theofilopoulos ◽  
H.O. McDevitt ◽  
A.B. Pereira ◽  
D. Carson ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Immune Complexes ◽  
Circulating Immune Complexes ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome

Increased Recovery of Klebsiella from the Gastrointestinal Tract of Reiter's Syndrome and Ankylosing Spondylitis Patients

Rheumatology ◽  
1983 ◽  
Vol XXII (suppl 2) ◽  
pp. 85-90 ◽  
Author(s):  
T. T. Kuberski ◽  
H. G. Morse ◽  
R. G. Rate ◽  
M. D. Bonnell
Keyword(s):  
Ankylosing Spondylitis ◽  
Gastrointestinal Tract ◽  
Reiter's Syndrome ◽  
Reiter’S Syndrome
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