Functional analysis of rheumatoid factor-producing B cells from the synovial fluid of rheumatoid arthritis patients

Reparon-Schuijt, Carelle C.; Esch, Wim J. E. van; Kooten, Cees van; Levarht, E. W. Nivine; Breedveld, Ferdinand C.; Verweij, Cornelis L.

doi:10.1002/1529-0131(199812)41:12<2211::aid-art17>3.0.co;2-o

Cited by 50 publications

(29 citation statements)

References 58 publications

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“…When anti-CD40L antibodies were given after the onset of clinically apparent disease, no effect on joint scores or ankle thickness could be seen. CD40L blockade may have prevented the emergence of new autoreactive B cells by facilitating their peripheral deletion, but the silencing of CD40 signaling may not have been as influential on the memory B cell or plasma cell populations (36). After a number of autoreactive clones escaped deletion, anti-CD40L treatment did not significantly reduce the antibody load.…”

Section: Discussionmentioning

confidence: 99%

The role of CD40 ligand and tumor necrosis factor α signaling in the transgenic K/BxN mouse model of rheumatoid arthritis

Kyburz

Carson

Corr

2000

Arthritis & Rheumatism

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Objective. Spontaneous arthritis in the KRN transgenic mouse (K/BxN) model is due to the auto-reactivity of the transgenic T cell receptor and subsequent induction of autoantibodies directed against glucose-6-phosphate isomerase (G6PI). This study sought to analyze the potential of anti-CD40 ligand (anti-CD40L) and anti-tumor necrosis factor (anti-TNF) antibodies in preventing and treating arthritis in this murine model. Methods. Groups of K/BxN mice were injected with anti-CD40L and anti-TNF antibodies during various stages of arthritis. Disease was assessed by clinical scoring, measurements of paw swelling, and histology. The results were correlated with the levels of autoanti-bodies in the serum, as assessed by enzyme-linked immunosorbent assay. Results. Anti-CD40L antibody treatment was able to diminish significantly the arthritis development in K/BxN mice when given a week before the onset of clinically apparent disease. However, no effect on disease was seen when the antibodies were administered after clinical onset. Surprisingly, neutralizing anti-TNF antibodies were unable to prevent arthritis in K/BxN mice. The success of antibody treatment in preventing disease correlated with low levels of anti-G6PI antibodies in the serum. Conclusion. These results suggest that anti-CD40L treatment can prevent arthritis development in a model of immunoglobulin-mediated arthritis, but anti-TNF treatment cannot. The unsuccessful treatment of established disease was possibly due to the continued presence of autoreactive antibodies in the arthritic mice.

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Section: Discussionmentioning

confidence: 99%

The role of CD40 ligand and tumor necrosis factor α signaling in the transgenic K/BxN mouse model of rheumatoid arthritis

Kyburz

Carson

Corr

2000

Arthritis & Rheumatism

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“…The immunoregulatory cytokine interleukin-10 (IL-10) increases autoantibody production by B cells from RA patients (1,2). IL-10 stimulates B cell survival, proliferation, differentiation, and antibody isotype switching (3).…”

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confidence: 99%

Association of the –2849 interleukin‐10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis

Lard¹,

Gaalen²,

Schonkeren³

et al. 2003

Arthritis & Rheumatism

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Objective. To analyze the -2849 A/G interleukin-10 (IL-10) promoter polymorphism, which is associated with high (AG/GG) and low (AA) IL-10 production, in a cohort of rheumatoid arthritis (RA) patients and controls in order to gain a better understanding of its role in the incidence and progression of RA.Methods. Allele frequencies of the promoter polymorphism -2849 A/G and carriage rates were compared in 283 RA patients, 413 patients with other rheumatic diseases, and 1,220 healthy controls. The rate of joint damage and baseline levels of IgG and IgM rheumatoid factors and anti-citrullinated peptide antibodies were measured and were correlated with the IL-10 gene polymorphism. Furthermore, the correlation between the invasiveness of fibroblast-like synoviocytes (FLS) and the ؊2849 IL-10 genotype was tested.

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“…The switched memory B cell pool is enlarged in RA patients, and CD38 + plasma-cell-like B cells are present in higher numbers [21]. The lower concentrations of sCD21 are most likely not related to properties of the peripheral blood B cell pool alone, since peripheral blood B cells from RA patients produce amounts of sCD21 comparable to those from healthy individuals [16].…”

Section: Discussionmentioning

confidence: 99%

Soluble CD21 in sera and synovial fluid of arthritic patients

et al. 2005

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Soluble CD21 (sCD21) is the ectodomain of the CD21 glycoprotein released by shedding from the cellular membrane. The ectodomain of CD21 is capable of binding complement fragments, Epstein-Barr virus (EBV) and CD23. Functionally sCD21 can activate monocytes and abrogate B-cell/follicular dendritic cell interaction, thereby inhibiting antibody production by antigen primed B cells. Levels of sCD21 vary in several clinical conditions. Here we analyzed sCD21 in synovial fluids and sera in arthritic patients. sCD21 concentrations were consistently lower in synovial fluids compared to paired sera samples from the same patients. In contrast to healthy donors, sCD21 levels are significantly reduced in rheumatoid arthritis patient's sera. Potential causes and consequences of the data are discussed.

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Functional analysis of rheumatoid factor-producing B cells from the synovial fluid of rheumatoid arthritis patients

Cited by 50 publications

References 58 publications

The role of CD40 ligand and tumor necrosis factor α signaling in the transgenic K/BxN mouse model of rheumatoid arthritis

The role of CD40 ligand and tumor necrosis factor α signaling in the transgenic K/BxN mouse model of rheumatoid arthritis

Association of the –2849 interleukin‐10 promoter polymorphism with autoantibody production and joint destruction in rheumatoid arthritis

Soluble CD21 in sera and synovial fluid of arthritic patients

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