scholarly journals A comparative study of HLA genes in HLA–B27 positive ankylosing spondylitis and HLA–B27 positive peripheral reactive arthritis

1996 ◽  
Vol 39 (6) ◽  
pp. 943-949 ◽  
Author(s):  
Pia Westman ◽  
Marjatta Leirisalo-Repo ◽  
Jukka Partanen ◽  
Saija Koskimies
Keyword(s):  
Ankylosing Spondylitis ◽  
Comparative Study ◽  
Reactive Arthritis ◽  
Hla B27 ◽  
Hla Genes

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.

Absence of cross-reaction between HLA B27 and yersinia enterocolitica or chlamydia trachomatis in reactive arthritis and ankylosing spondylitis

1985 ◽  
Vol 4 (4) ◽  
pp. 487-487 ◽  
Author(s):  
J. Roudier ◽  
H. De Montclos ◽  
D. Thouvenot ◽  
J. J. Chomel ◽  
F. N. Guillermet ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Chlamydia Trachomatis ◽  
Yersinia Enterocolitica ◽  
Reactive Arthritis ◽  
Cross Reaction ◽  
Hla B27

Influence of HLA-B*5703 and HLA-B*1403 on Susceptibility to Spondyloarthropathies in the Zambian Population

2008 ◽  
Vol 35 (11) ◽  
pp. 2236-2240 ◽  
Author(s):  
ROBERTO DÍAZ-PEÑA ◽  
MIGUEL ANGEL BLANCO-GELAZ ◽  
PANGANANI NJOBVU ◽  
ANTONIO LÓPEZ-VAZQUEZ ◽  
BEATRIZ SUÁREZ-ÁLVAREZ ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Ankylosing Spondylitis ◽  
Reactive Arthritis ◽  
Hiv Positive ◽  
Sample Population ◽  
Type I ◽  
Hla B27 ◽  
New Findings ◽  
Immunodeficiency Virus ◽  
Sub Saharan

ObjectiveTo analyze the distribution of HLA-B alleles and to investigate their contribution in the susceptibility to spondyloarthropathies (SpA) in a sample population from Zambia, in order to determine a relationship between some HLA-B alleles and development of ankylosing spondylitis (AS), reactive arthritis (ReA), or undifferentiated SpA (uSpA).MethodsWe selected 72 patients with SpA and found that 46 had uSpA, 23 ReA, and 3AS.We also selected 92 matched controls; 55 of these had human immunodeficiency virus type I (HIV-I) infection.ResultsWe found a significant increase in the rate of uSpA and ReA with features of Reiter’s syndrome (RS) in HIV-positive individuals who carried the HLA-B*5703 allele (pc < 0.0001 and pc < 0.001, respectively). Among the significant new findings identified were the presence of B*1403 in 2 of the 3 AS patients (pc < 0.05, OR 47), confirming previous data in the Togolese population.ConclusionThe presence of B*5703 and HIV infection may not affect susceptibility to AS and ReA, but they do show an important influence in uSpA and RS. Our findings confirm that HLA-B* 1403 is the only factor to increase the risk of AS in a sub-Saharan African population, whereas HLA-B27 was virtually absent in patients with AS.

HLA-B27-restricted CD8 T cells derived from synovial fluids of patients with reactive arthritis and ankylosing spondylitis

The Lancet ◽  
1993 ◽  
Vol 342 (8872) ◽  
pp. 646-650 ◽  
Author(s):  
E. Hermann ◽  
K-H. Meyer zum Büschenfelde ◽  
B. Fleischer ◽  
D.T.Y. Yu
Keyword(s):  
T Cells ◽  
Ankylosing Spondylitis ◽  
Cd8 T Cells ◽  
Reactive Arthritis ◽  
Hla B27 ◽  
Synovial Fluids

TAP1 and TAP2 polymorphism in HLA-B27-positive subpopulations: no allelic differences in ankylosing spondylitis and reactive arthritis

1995 ◽  
Vol 44 (4) ◽  
pp. 236-242 ◽  
Author(s):  
Pia Westman ◽  
Jukka Partanen ◽  
Marjatta Leirisalo-Repo ◽  
Saija Koskimies
Keyword(s):  
Ankylosing Spondylitis ◽  
Reactive Arthritis ◽  
Hla B27 ◽  
Allelic Differences

Distribution of HLA-B27 and its alleles in patients with reactive arthritis and with ankylosing spondylitis in Tunisia

2009 ◽  
Vol 29 (10) ◽  
pp. 1193-1196 ◽  
Author(s):  
Mariam Siala ◽  
Nadia Mahfoudh ◽  
Radhouane Gdoura ◽  
Mohamed Younes ◽  
Hela Fourati ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Reactive Arthritis ◽  
Hla B27

scholarly journals Pathogenicity of Misfolded and Dimeric HLA-B27 Molecules

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Antony N. Antoniou ◽  
Izabela Lenart ◽  
David B. Guiliano
Keyword(s):  
Animal Model ◽  
Ankylosing Spondylitis ◽  
Autoimmune Disease ◽  
Disease Progression ◽  
Chronic Inflammation ◽  
Reactive Arthritis ◽  
Potential Role ◽  
Biochemical Data ◽  
Hla B27 ◽  
Cellular Events

The association between HLA-B27 and the group of autoimmune inflammatory arthritic diseases, the spondyloarthropathies (SpAs) which include ankylosing spondylitis (AS) and Reactive Arthritis (ReA), has been well established and remains the strongest association between any HLA molecule and autoimmune disease. The mechanism behind this striking association remains elusive; however animal model and biochemical data suggest that HLA-B27 misfolding may be key to understanding its association with the SpAs. Recent investigations have focused on the unusual biochemical structures of HLA-B27 and their potential role in SpA pathogenesis. Here we discuss how these unusual biochemical structures may participate in cellular events leading to chronic inflammation and thus disease progression.

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