Effect of H-2 Genes on Expression of HLA-B27 and<i>Yersinia</i>-induced Arthritis

Nickerson, C. L.; Hogen, K. L.; Luthra, Harvinder S.; David, Chella S.

doi:10.3109/03009749009097063

Cited by 8 publications

(4 citation statements)

References 16 publications

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“…Despite intensive research in this area, the pathologic mechanism of AS is unknown. Studies on putative autoantigens implicated the role of molecular mimicry, represented by Klebsiella antigens (32,33), Yersinia antigens (34,35), self-recognized HLA-B27 (35-37), or epitopes in cartilage PG (38)(39)(40)(41) or versican (42). The present study could not reveal which subdomains within the murine H-2 locus are responsible and/or involved in the genetic predisposition to PGIS in either of the F 2 hybrids of BALB/c ϫ C3H or the BALB/c ϫ DBA/2 intercross.…”

Section: Discussionmentioning

confidence: 99%

Genetic control of experimental spondylarthropathy

Szabó

Szántó

Végvári

et al. 2005

Arthritis & Rheumatism

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PGIS, a murine model of autoimmune spondylitis, shows similarities to ankylosing spondylitis. Segregation of susceptibility to PG-induced arthritis (PGIA) from that to PGIS in different genetic crosses suggests that PGIA and PGIS are separate diseases. Therefore, this model allows for the elucidation of genetic components involved in the etiology of SpA, independent of those controlling the susceptibility to PGIA.

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Section: Discussionmentioning

confidence: 99%

Genetic control of experimental spondylarthropathy

Szabó

Szántó

Végvári

et al. 2005

Arthritis & Rheumatism

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“…The strong association between self-recognized human leukocyte antigen B27 (HLA-B27) and susceptibility to AS has been proposed over the past three decades; however, most individuals who test positive for HLA-B27 are healthy, thus the pathogenic mechanism underlying this association remains unclear. In addition, other putative autoantigens have been implicated in the etiology of AS, including Klebsiella antigens 3 , Yersinia antigens 4 . and epitopes in the cartilage PG 5 .…”

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confidence: 99%

Inhibition of Complement Retards Ankylosing Spondylitis Progression

Yang

Ding

Wang

et al. 2016

Sci Rep

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Ankylosing spondylitis (AS) is a chronic axial spondyloarthritis (SpA) resulting in back pain and progressive spinal ankyloses. Currently, there are no effective therapeutics targeting AS largely due to elusive pathogenesis mechanisms, even as potential candidates such as HLA-B27 autoantigen have been identified. Herein, we employed a proteoglycan (PG)-induced AS mouse model together with clinical specimens, and found that the complement system was substantially activated in the spinal bone marrow, accompanied by a remarkable proportion alteration of neutrophils and macrophage in bone marrow and spleen, and by the significant increase of TGF-β1 in serum. The combined treatment with a bacteria-derived complement inhibitor Efb-C (C-terminal of extracellular fibrinogen-binding protein of Staphylococcus aureus) remarkably retarded the progression of mouse AS by reducing osteoblast differentiation. Furthermore, we demonstrated that two important modulators involved in AS disease, TGF-β1 and RANKL, were elevated upon in vitro complement attack in osteoblast and/or osteoclast cells. These findings further unravel that complement activation is closely related with the pathogenesis of AS, and suggest that complement inhibition may hold great potential for AS therapy.

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“…Although transgenic rats that carry the HLA-B27 gene develop arthritis (32), transgenic mice carrying the same gene developed hindlimb paralysis, only after inoculation with Yersiniu enterocolitica 0:8 (33)(34)(35). No histopathologic findings in these animals have been reported in detail, except for spinal or paraspinal abscess formation.…”

Section: Discussionmentioning

confidence: 98%

Inflammatory polyarthritis in mice transgenic for human t cell leukemia virus type i

Yamamoto

Sekiguchi

Itagaki

et al. 1993

Arthritis & Rheumatism

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Objective. We have recently reported that arthropathy develops in high incidence among transgenic mice carrying the pX region of human T cell leukemia virus type I (HTLV-I). In the present study, the histopathologic features of the joints in these mice were examined in order to compare the animal disease with rheumatoid arthritis (RA) in humans.Methods. Paraffin sections of limbs (right and left fingers, wrists, elbows, shoulders, toes, knees, and ankles) were stained with hematoxylin and eosin, periodic acidachiff, azan-Mallory, or phosphotungstic acid hematoxylin, and examined by light microscopy.Results. Abnormalities of the limbs began to occur as early as 3 weeks of age, and the incidence gradually increased until the mice were 12 months old. The incidence of arthropathy was 22% (48 of 217) at 3 months of age and 28% (18 of 64) at 6 months. The

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Effect of H-2 Genes on Expression of HLA-B27 andYersinia-induced Arthritis

Cited by 8 publications

References 16 publications

Genetic control of experimental spondylarthropathy

Genetic control of experimental spondylarthropathy

Inhibition of Complement Retards Ankylosing Spondylitis Progression

Inflammatory polyarthritis in mice transgenic for human t cell leukemia virus type i

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