Aberrant TNF secretion by whole blood in healthy subjects with a history of reactive arthritis: time course in adherent and non-adherent cultures

Anttonen, Krista; Orpana, Arto; Leirisalo‐Repo, Marjatta; Repo, Heikki

doi:10.1136/ard.2005.035972

Cited by 14 publications

(6 citation statements)

References 31 publications

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“…In addition, the arthritogenicity of Y. enterocolitica serotype O:3, the most frequently occurring human arthritogenic serotype, has not been studied in TNFRp55À/À mice. Furthermore, since abnormality of TNF-level has been detected in patients with ReA [3], the results presented here could be extrapolated to human ReA.…”

Section: Introductionmentioning

confidence: 85%

“…There is increasing evidence that TNF-genotypes which seem to be associated with low TNF-production are present at a higher percentage in ReA [2]. Moreover, aberrant TNF secretion has been recently reported in subjects with previous Yersinia-triggered ReA [3]. TNF mediates pleiotropic activities via two surface receptors, TNFRp55 (TNFR1, CD120a) and TNFRp75 (TNFRII, CD120b).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response

Genaro

Cargnelutti²,

Eliçabe³

et al. 2006

Rheumatology

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Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response

Genaro

Cargnelutti²,

Eliçabe³

et al. 2006

Rheumatology

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“…These cytokines may be released by visceral fat, but also by fat that surrounds blood vessels [8]. TNFa has been reported to have a role in the production of both pain [55 -57] and pathology, and of course is the key cytokine in systemic spondyloarthropathy, a bone-tendon junction disease [58,59]. Adipocytokines also include substances that may be beneficial for tendon health, such as transforming growth factor beta and insulin-like growth factor 1, and further research needs to clarify whether and which adipocytokines may be involved in tendon health.…”

Section: Potential Mechanisms For the Associationmentioning

confidence: 99%

Adiposity and tendinopathy

Gaida¹,

Cook²,

Bass³

2008

Disability and Rehabilitation

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“…However, TNF has also been considered a critical cytokine capable of activating macrophages during the protective host response against bacterial infections, such as Y. enterocolitica (5). Interestingly, low TNF production has been detected in sera of a high percentage of patients with ReA (6,7). Given the dual role of TNF as a pathogenic or hostprotective factor in autoimmune or microbial settings, the pathological relevance of this cytokine in ReA remains unclear.…”

mentioning

confidence: 99%

Lack of TNFR p55 Results in Heightened Expression of IFN-γ and IL-17 during the Development of Reactive Arthritis

Eliçabe¹,

Cargnelutti²,

Serer³

et al. 2010

The Journal of Immunology

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Reactive arthritis (ReA) is a type of arthritis originating from certain gastrointestinal or genitourinary infections. In previous studies, we reported the development of progressive Yersinia enterocolitica-induced ReA in mice lacking TNFR p55; however, the mechanisms underlying this effect are still uncertain. In this study, we investigated the impact of TNFR p55 deficiency in modulating Ag-specific Th1 and Th17 responses during this arthritogenic process. We found more severe ReA in TNFRp55−/− mice compared with their wild-type (WT) counterparts. This effect was accompanied by increased levels of Yersinia LPS in the joints of knockout mice. Analysis of the local cytokine profile revealed greater amounts of IFN-γ and IL-17 in arthritic joints of TNFRp55−/− mice compared with WT mice at day 21 postinfection. Moreover, altered IL-17 and IFN-γ production was observed in mesenteric and inguinal lymph nodes of Yersinia-infected TNFRp55−/− mice, as well as in spleen cells obtained from infected mice and restimulated ex vivo with bacterial Ags. Increased levels of cytokine secretion were associated with a greater frequency of CD4+IL-17+, CD4+IFN-γ+, and IL-17+IFN-γ+ cells in TNFRp55−/− mice compared with WT mice. Remarkably, Ab-mediated blockade of IL-17 and/or IFN-γ resulted in reduced joint histological scores in TNFRp55−/− mice. A mechanistic analysis revealed the involvement of p40, a common subunit of heterodimeric IL-12 and IL-23, in the generation of augmented IFN-γ and IL-17 production under TNFR p55 deficiency. Taken together, these data indicate that, in the absence of TNFR p55 signaling, Th1 and Th17 effector cells may act in concert to sustain the inflammatory response in bacterial-induced arthritogenic processes.

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Aberrant TNF secretion by whole blood in healthy subjects with a history of reactive arthritis: time course in adherent and non-adherent cultures

Abstract: who have recovered from yersinia arthritis show enhanced TNF production, which may be regulated at the level of monocyte adhesion.

Cited by 14 publications

References 31 publications

Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response

Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response

Adiposity and tendinopathy

Lack of TNFR p55 Results in Heightened Expression of IFN-γ and IL-17 during the Development of Reactive Arthritis

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