Induction of type B synoviocyte-like cells from plasmacytoid dendritic cells of the bone marrow in rheumatoid arthritis and osteoarthritis

Hirohata, Shunsei; Nagai, Tatsuo; Asako, Kurumi; Tomita, Tadanori; Yoshikawa, Hideki

doi:10.1016/j.clim.2011.04.008

Cited by 15 publications

(10 citation statements)

References 25 publications

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“…Since type B synoviocytes have also been shown to express TNF-α like monocytes on their surface [13], it is possible that infliximab and etanercept might bind and deliver signals leading to degeneration or apoptosis. On the other hand, recent studies have shown that differentiation of type B synoviocytes requires the action of TNF-α [16, 17]. Therefore, it is also possible that inhibition of TNF-α might suppress the differentiation of type B synoviocytes within the synovium, leading to the loss or decreased stratification of synovial lining cells.…”

Section: Discussionmentioning

confidence: 99%

TNF inhibitors induce discoid fibrosis in the sublining layers of the synovium with degeneration of synoviocytes in rheumatoid arthritis

et al. 2013

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We determined the characteristic features of synovial tissues of rheumatoid arthritis (RA) patients treated by TNF inhibitors in order to delineate their mechanism of action. Synovial tissues were obtained during the joint surgical operations from 12 RA patients who had been treated with TNF inhibitors in addition to disease modifying antirheumatic drugs (DMARDs) for at least 5 months (5–25 months) (RA-TNFinh), and from 12 RA patients who had been treated with DMARDs alone (RA-DMARD), and were evaluated under light microscopy. There were no significant differences in disease duration, serum CRP levels, DAS28, Steinbrocker’s stages on X-ray and treatment regimen except for TNF inhibitors between RA-TNFinh and RA-DMARD. The most prominent changes in the synovium from RA-TNFinh were discoid fibrosis in the subliming layers of the synovium with degeneration and detachment of synoviocytes and marked decrease in vasculatures. There was no significant difference in these synovial features between RA patients with infliximab and those with etanercept. Interestingly, appearance of osteoclasts was observed in RA-TNFinh (3 out of 12 patients) and in RA-DMARD (1 out of 12 patients). These results indicate that not only infliximab, but etanercept might have direct actions on synovial cells in the deep lining layers of the synovium, leading to the discoid fibrosis thereof. Moreover, the data confirm that the deep lining or sublining layers of the synovium are the most important portions that steer the disease process of RA synovitis.

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Section: Discussionmentioning

confidence: 99%

TNF inhibitors induce discoid fibrosis in the sublining layers of the synovium with degeneration of synoviocytes in rheumatoid arthritis

et al. 2013

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“…On the other hand, it has been demonstrated that cadherin-11 is abundantly expressed in type B synoviocytes (Chang et al,2010) compared with lung or dermal fibroblasts (Vandooren et al,2008). Accordingly, the FLC induced from RA and OA bone marrow pDC expressed comparable amounts of cadherin-11 mRNA to RA and OA synovial FLC (Hirohata et al,2011). These results indicate that DC are one of the progenitors of type B synoviocytes irrespective of RA or OA and suggest that bone marrow CD34+ cells might differentiate into type B synoviocyte-like cells via DC, since DC have been demonstrated to originate from CD34+ cells (Reid et al,1992;Szabolcs et al,1995;Chen et al,2004).…”

Section: Capacity Of Bone Marrow DC To Differentiate Into Type B Synomentioning

confidence: 85%

“…Apparently, RA bone marrow CD34+ cells have abnormal mRNA expression for several genes, possibly resulting in abnormal differentiation of monocytes and DC. Moreover, it is strongly suggested that DC, as precursors for synovial fibroblasts, might also contribute to the spread of destructive arthritis between joints in RA (Hirohata et al,2011;Lefèvre et al,2009). Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Of note, depletion of pDC from RA bone marrow CD34+ cells significantly diminished their capacities to differentiate into FLC, which were restored by addition of pDC in a dose-response manner (Hirohata et al,2011). It should be pointed out that generation of FLC from RA bone marrow CD34+ cells or pDC was correlated with MMP-1 levels in culture supernatants (Hirohata et al,2001;Hirohata et al,2011).…”

Section: Capacity Of Bone Marrow DC To Differentiate Into Type B Synomentioning

confidence: 99%

“…We have recently demonstrated that bone marrow plasmacytoid DC (pDC) as well as myeloid DC (mDC), irrespective of their origin from RA bone marrow or osteoarthritis (OA) bone marrow, have prominent capacity to differentiate into FLC producing MMP-1 especially under influences of TNF-α (Hirohata et al,2011). Of note, depletion of pDC from RA bone marrow CD34+ cells significantly diminished their capacities to differentiate into FLC, which were restored by addition of pDC in a dose-response manner (Hirohata et al,2011).…”

Section: Capacity Of Bone Marrow DC To Differentiate Into Type B Synomentioning

confidence: 99%

See 2 more Smart Citations

Role of Bone Marrow in the Pathogenesis of Rheumatoid Arthritis

Hirohata¹

2011

Challenges in Rheumatology

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Cadherin-11 mRNA transcripts are frequently found in rheumatoid arthritis peripheral blood and correlate with established polyarthritis

Sfikakis

Christopoulos

et al. 2014

Clinical Immunology

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Rheumatoid arthritis (RA) synovial fibroblasts hyperexpress the mesenchymal cadherin-11, which is involved also in tumor invasion/metastasis, whereas anti-cadherin-11 therapeutics prevent and reduce experimental arthritis. To test the hypothesis that cadherin-11 is aberrantly expressed in RA peripheral blood, 100 patients (15 studied serially) and 70 healthy controls were analyzed by real-time reverse transcription-PCR. Cadherin-11 mRNA transcripts were detected in 69.2% of moderately/severely active RA, versus 31.8% of remaining patients (p=0.001), versus 17.1% of controls (p<0.0001). Notably, cadherin-11 positivity correlated significantly and independently only with established (>1year) polyarthritis (>4 swollen tender joints), by multivariate logistic regression analysis including various possible clinical/laboratory factors. Rare cells of undefined nature, detected by flow cytometry following CD45(-) enrichment, strongly expressed surface cadherin-11 (estimated 10-50cells/ml of blood) in 5/6 patients with polyarticular established disease versus 1/6 patients with early RA. Studies on the potential pathogenic role of circulating cells expressing cadherin-11 in RA are warranted.

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Induction of type B synoviocyte-like cells from plasmacytoid dendritic cells of the bone marrow in rheumatoid arthritis and osteoarthritis

Cited by 15 publications

References 25 publications

TNF inhibitors induce discoid fibrosis in the sublining layers of the synovium with degeneration of synoviocytes in rheumatoid arthritis

TNF inhibitors induce discoid fibrosis in the sublining layers of the synovium with degeneration of synoviocytes in rheumatoid arthritis

Role of Bone Marrow in the Pathogenesis of Rheumatoid Arthritis

Cadherin-11 mRNA transcripts are frequently found in rheumatoid arthritis peripheral blood and correlate with established polyarthritis

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