Familial rheumatoid arthritis: linkage of HLA to disease susceptibility locus in four families where proband presented with juvenile rheumatoid arthritis.

Rossen, Roger D.; Brewer, Earl J.; Sharp, R. Mark; Ott, J.; Templeton, Joe W.

doi:10.1172/jci109708

Cited by 34 publications

(10 citation statements)

References 41 publications

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“…Anecdotal evidence suggests that families with JRA probands have an additional, and perhaps stronger, risk of other nonrheumatic autoimmune diseases. Other forms of arthritis and other autoimmune diseases, including alopecia areata, insulindependent diabetes mellitus, thyroid disease, vitiligo, and autoimmune oophoritis, have all been reported in families with a JRA proband (13)(14)(15). It is unclear whether the rates of occurrence of these autoimmune disorders are above those that are to be expected based on the rates in the general population.…”

Section: Epidemiology and Demographicsmentioning

confidence: 99%

Juvenile rheumatoid arthritis as a complex genetic trait

Glass

Giannini

1999

Arthritis & Rheumatism

179

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Section: Epidemiology and Demographicsmentioning

confidence: 99%

Juvenile rheumatoid arthritis as a complex genetic trait

Glass

Giannini

1999

Arthritis & Rheumatism

179

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“…Although rheumatoid and severe Lyme arthritis are characterized by similar cellular infiltrates, 4,7,[21][22][23] there are important characteristics that suggest they could be regulated by different mechanisms. In rodent models rheumatoid arthritis is absolutely linked to particular alleles of the MHC, 40,41 requires T cells that recognize self-antigens such as collagen presented by the MHC susceptibility allele, 42 and involves antibodies to these self-antigens. Lyme arthritis is unique in that it develops in scid and rag mice, [43][44][45][46] indicating that the adaptive immune response is not required for the initiation of arthritis.…”

Section: Discussionmentioning

confidence: 99%

Bb2Bb3 Regulation of Murine Lyme Arthritis Is Distinct from Ncf1 and Independent of the Phagocyte Nicotinamide Adenine Dinucleotide Phosphate Oxidase

Crandall

Dunn

et al. 2005

The American Journal of Pathology

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Several quantitative trait loci regulating murine Lyme arthritis severity have been mapped, including a highly significant linkage found on chromosome 5, termed Bb2Bb3. Within this region, the Ncf1 gene of the phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase has recently been identified as a major regulator of arthritis severity in rodent models of rheumatoid arthritis, an effect attributed to protective properties of reactive oxygen species. To assess the role of Ncf1 in Lyme arthritis, we introgressed Bb2Bb3 from severely arthritic C3H/He mice onto mildly arthritic C57BL/6 mice. This increased Lyme arthritis severity, whereas the reciprocal transfer conferred protection from disease. A single nucleotide polymorphism was identified in the Ncf1 gene that did not influence the protein sequence or expression of Ncf1. Although polymorphonuclear leukocytes from C57BL/6 mice generated a greater oxidative burst than polymorphonuclear leukocytes from C3H/He mice, studies with the Bb2Bb3 congenic mice demonstrated this difference was not linked to Ncf1 alleles. Furthermore, Lyme arthritis severity was not altered in mice lacking either the Ncf1 or Gp91phox subunits of the NADPH oxidase complex. Together, these results argue that Ncf1 is not a candi- Lyme disease is caused by the tick-borne spirochete Borrelia burgdorferi and can involve multiple organs including the joints, heart, skin, and nervous system. 1 Lyme arthritis is a consequence of bacterial invasion of joint tissue and results from localized inflammation triggered by persistent infection. 2,3 Arthritis develops weeks to months after transmission from an infected tick and is characterized by edema, inflammatory cell infiltration, and hyperproliferation of synovium. 1,4,5 In most individuals, arthritis will resolve after clearance of the bacteria, however, a subset of individuals with the most severe inflammatory arthritis have been documented to develop treatment-resistant arthritis that does not respond to antibiotic therapy. 6,7 It is suspected that in these individuals progression to an autoimmune-mediated arthritis more similar to rheumatoid arthritis has occurred. Susceptibility to treatment-resistant arthritis is associated with HLA-DR1*0401, a major histocompatibility complex (MHC) class II allele also associated with rheumatoid arthritis. 6,8,9 These studies suggest that there are two distinct stages of Lyme arthritis; an acute inflammatory arthritis dependent on bacterial invasion and persistence in joint tissues and a chronic, treatment-resistant arthritis that may represent a transition to a rheumatoid-like disease.

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“…Более 50 различных работ из разных стран мира подтвердили роль полиморфизма антигенов гисто совместимости в развитии заболевания [8, 9,10,11,1 2, 13,14,15,16,17,18,19,20].…”

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“…Выявлены ассоциации с HLA Dw4, DR-1, DR-4, которые рассматриваются как факто ры риска развития полиартикулярного начала ЮРА [17,27,46,48,49]. Сильная ассоциация выявляется между серопозитивным по РФ полиартритом и DR-4.…”

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