Synovial fluid in ankylosing spondylitis.

Kendall, M. J.; Farr, M.; Meynell, M. J.; Hawkins, C F

doi:10.1136/ard.32.6.487

Cited by 24 publications

(6 citation statements)

References 20 publications

(18 reference statements)

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“…Neutrophils are associated with the AS inflammation, since an increased proportion of peripheral neutrophils has been suggested as an indicator of disease activity [18,19]. Moreover, neutrophils accumulate in the synovial fluid of AS patients and infiltrate inflamed entheses [32,33]. These neutrophils are thought to be active and tissue toxic, by releasing proteases, ROS and proinflammatory cytokines that contribute to chronic arthritis and ultimately bone damage [34].…”

Section: Discussionmentioning

confidence: 99%

IL‐17A expressed on neutrophil extracellular traps promotes mesenchymal stem cell differentiation toward bone‐forming cells in ankylosing spondylitis

et al. 2021

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Ankylosing spondylitis (AS) is an inflammatory disease characterized by excessive bone formation. We investigated the presence of neutrophil extracellular traps (NETs) in AS and how they are involved in the osteogenic capacity of bone marrow mesenchymal stem cells (MSCs) through interleukin‐17A (IL‐17A). Peripheral neutrophils and sera were obtained from patients with active AS and healthy controls. NET formation and neutrophil/NET‐associated proteins were studied using immunofluorescence, immunoblotting, qPCR, and ELISA. In vitro co‐culture systems of AS NET structures and MSCs isolated from controls were deployed to examine the role of NETs in the differentiation of MSCs toward osteogenic cells. Analysis was performed using specific staining and qPCR. Neutrophils from patients with AS were characterized by enhanced formation of NETs carrying bioactive IL‐17A and IL‐1β. IL‐17A‐enriched AS NETs mediated the differentiation of MSCs toward bone‐forming cells. The neutrophil expression of IL‐17A was positively regulated by IL‐1β. Blocking IL‐1β signaling on neutrophils with anakinra or dismantling NETs using DNase‐I disrupted osteogenesis driven by IL‐17A‐bearing NETs. These findings propose a novel role of neutrophils in AS‐related inflammation, linking IL‐17A‐decorated NETs with the differentiation of MSCs toward bone‐forming cells. Moreover, IL‐1β triggers the expression of IL‐17A on NETs offering an additional therapeutic target in AS.

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Section: Discussionmentioning

confidence: 99%

IL‐17A expressed on neutrophil extracellular traps promotes mesenchymal stem cell differentiation toward bone‐forming cells in ankylosing spondylitis

et al. 2021

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“…So far, no correlation has been found (Dausset & Hors Sachs et al 1975, . There is, however, increasing evidence to suggest that the immune response may play an important part in the aeti-ology and pathogenesis of the disease (Veys & Van Laere 1973, Kendall et al 1973, Eghtedari et al 1976). Recently, a diminished mixed lymphocyte response among ankylosing spondylitic patients has been reported (Nikbin et al 1975(Nikbin et al , 1976, and this has been interpreted as indicating a defect in cell-mediated immunity.…”

Section: Received For Publication 19 August Accepted 19 August 1977mentioning

confidence: 99%

Diminished Mixed Lymphocyte Response in Ankylosing Spondylitis

Wee

Daymond

1978

Tissue Antigens

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A diminished mixed lymphocyte response was reported by Nikbin et al. (1976) among patients with ankylosing spondylitis, their asymptomatic relatives and also normal controls carrying the B27 antigen. In the present communication, the responses in 48 ankylosing spondylitis patients and 45 controls were examined in mixed lymphocyte cultures tested against a 'standard stimulator' made up of pooled lymphocytes. A significantly diminished response is confirmed among the ankylosing spondylitis patients, but not in the control group carrying the B27 antigen. The diminished mixed lymphocyte response therefore appears to be more directly associated with the disease than with the B27 antigen, and possibly represents a specific T-cell defect associated with the pathogenesis of the disease.

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“…We subsequently discovered that MIF enhanced the frequency of RORγt + FOXP3 + T regs in both mice and humans in vitro, and also identified that SpA patients had T regs exhibiting a T H 17 cell–like phenotype in both blood and SF, demonstrating the potential of MIF to enhance type 3 immunity in SpA. Given that neutrophils are the most abundant cells in SF of inflamed joints ( 38 ) and concentrations of MIF in serum and SF of SpA patients are higher than those of healthy or disease controls ( 5 ), MIF predominantly produced by neutrophils may boost type 3 immunity in patients with SpA by enhancing T reg acquisition of a T H 17 cell–like phenotype.…”

Section: Discussionmentioning

confidence: 96%