Few human autoimmune sera detect GPI

Kassahn, Daniela; Kolb, Cornelia; Solomon, Samuel; Bochtler, Petra; Illges, Harald

doi:10.1038/ni0502-411b

Cited by 57 publications

(39 citation statements)

References 6 publications

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“…GPI is a ubiquitous protein that has been found to precipitate in the synovial lining layer on cartilage surface of mice and shown to be a jointspecific target for arthritogenic antibodies [32]. However, the occurrence of anti-GPI antibodies in RA remains to be clearly demonstrated [33,34]. Whereas the classical pathway seems to be of critical importance in our experiment using anti-CII antibodies, the reasons for it playing no role in the development of anti-GPI antibody-induced arthritis could be severalfold.…”

Section: Discussionmentioning

confidence: 99%

Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis

et al. 2004

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To analyze the role of the classical and alternative pathways of complement activation in the effector phase of arthritis, we have induced arthritis in C3-and factor B (FB)-deficient (C3 -/-and FB -/-) DBA/1J mice using well-defined monoclonal IgG2b and IgG2a antibodies to type II collagen. In control DBA/1J mice, severe swelling of the joints, destruction of cartilage and erosion of bone developed very rapidly with a 100% incidence and a peak on days 7-10. Although 75% of C3 -/-mice developed arthritis, the clinical severity was very mild and the onset was delayed. Severity of arthritis in FB -/-mice ranked intermediate in comparison with C3 -/-and control mice with an incidence of 100%. Immunohistochemical analysis of the inflamed joints demonstrated substantial reduction in macrophage and neutrophilic leukocyte infiltration in both C3 -/-and FB -/-mice, thereby confirming the clinical findings. We conclude that both the classical and the alternative pathways of complement activation are involved in the effector phase of arthritis.

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Section: Discussionmentioning

confidence: 99%

Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis

et al. 2004

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“…However, several other observations did not support this conception [10][11][12][13]. Kassahn et al reported that few human autoimmune sera were detected with G6PI [10].…”

Section: Introductionmentioning

confidence: 77%

“…Kassahn et al reported that few human autoimmune sera were detected with G6PI [10]. Herve et al found that G6PI was not a specific autoantigen in RA [12].…”

Section: Introductionmentioning

confidence: 99%

The diagnostic significance of glucose-6-phosphate isomerase (G6PI) antigen and anti-G6PI antibody in rheumatoid arthritis patients

Yang¹,

Ge²,

Dong³

et al. 2013

ABB

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Objective: To investigate whether glucose-6-phosphate isomerase (G6PI) antigen and anti-G6PI antibodies could be applied for the clinical diagnostic markers of rheumatoid arthritis (RA) and its associations with RA activity states. Methods: The levels of G6PI antigens and anti-G6PI Abs in sera from 176 RA patients in different states, 35 non-RA patients and 100 healthy donors and in synovia fluids from 33 patients and 11 non-RA patients were measured by ELISA. Results: The sensitivity and specificity of G6PI antigens in the RA patients were 75.0% and 93.3%, respectively. The levels of serum G6PI antigens in 176 RA patients were significantly higher than non-RA patients and the health controls. Especially, there was a significant difference between the active phase and the inactive phase in G6PI antigens levels. The levels of G6PI antigens in synovia fluid were also significantly higher in RA groups than in non-RA patients. With the values of the anti-G6PI Abs in sera, there were no marked differences among RA, non-RA patients and health controls. Also, there was no significant difference between the active phase and the inactive phase in RA patients. However, there were no significant differences of G6PI and anti-G6PI between RA patients and health controls in synovial fluid. Conclusions: G6PI is highly correlated with the activity states of RA, and could be applied for a clinical biomarker with high sensitivity and specificity for the diagnosis of RA.

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“…It has been reported that GPI is an autoantigen in RA, being present in 64% of patients but only a few healthy control subjects (4). However, the notion that GPI is an autoantigen in RA is surrounded by controversy, since a number of other groups of investigators could not reproduce these observations (5,6).…”

mentioning

confidence: 99%

Association of autoantibodies to glucose‐6‐phosphate isomerase with extraarticular complications in rheumatoid arthritis

Gaalen

Toes

Ditzel

et al. 2004

Arthritis & Rheumatism

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Objective. In the K/BxN mouse model, autoantibodies against glucose-6-phosphate isomerase (GPI) cause arthritis. The relevance of this model for human disease remains a subject of controversy. We set out to determine whether GPI autoantibodies occur in patients with rheumatoid arthritis (RA) and, if so, at what stage of the RA.Methods. Using an enzyme-linked immunosorbent assay, serum from 131 RA patients and 28 healthy controls was tested for autoantibodies against recombinant human GPI. Patients were grouped according to disease duration and presence of rheumatoid nodules, rheumatoid vasculitis, and Felty's syndrome, which are extraarticular complications of RA.Results. Elevated levels of autoantibodies against GPI were present in 5% of patients with uncomplicated RA and 4% of controls. In RA complicated by extraarticular manifestations, anti-GPI antibodies were observed in 18% of patients with rheumatoid nodules, 45% of patients with rheumatoid vasculitis, and 92% of patients with Felty's syndrome.Conclusion. In patients with RA, autoantibodies to GPI are associated with the occurrence of extraarticular complications.

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Few human autoimmune sera detect GPI

Cited by 57 publications

References 6 publications

Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis

Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis

The diagnostic significance of glucose-6-phosphate isomerase (G6PI) antigen and anti-G6PI antibody in rheumatoid arthritis patients

Association of autoantibodies to glucose‐6‐phosphate isomerase with extraarticular complications in rheumatoid arthritis

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