Update on cytokines in rheumatoid arthritis

Brennan, Fionula M.; Beech, Jonathan T

doi:10.1097/bor.0b013e32805e87f1

Cited by 75 publications

(57 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The role of several cytokines and chemokines in the pathogenesis of RA is well established [Brennan and Beech, 2007;McInnes and Schett, 2007], and this has led to progress in developing therapeutic strategies against this disease McInnes and Schett, 2007;Mitchell and Pisetsky, 2007]. Despite the different etiologies of infectious and autoimmune arthritides, our results reveal remarkable similarities between macrophage responses induced by SinV infection and those observed in RA.…”

Section: Remarkable Similarities Between Macrophage Responses In Sinvmentioning

confidence: 46%

Pro‐inflammatory response resulting from sindbis virus infection of human macrophages: Implications for the pathogenesis of viral arthritis

Assunção‐Miranda

Bozza

Poian

2009

Journal of Medical Virology

View full text Add to dashboard Cite

Several viruses cause acute and chronic joint inflammation in humans, and among them, the alphaviruses are of special interest due to the increasing number of outbreaks in which they are the etiological factor. Sindbis virus (SinV), a member of the Alphavirus genus, is the most widely distributed of all known arboviruses. Although SinV causes arthritis in humans, the molecular and cellular factors that contribute to the pathogenesis of this disease are almost completely unknown. Despite the crucial role of macrophages in the development of arthritis, these cells have not been recognized as potential targets for viruses causing arthritis. In this study, replication of SinV in human macrophages was demonstrated. The infection promoted macrophage activation, leading to the release of macrophage migration inhibitor factor (MIF) from intracellular stores and inducing the expression and secretion of TNF-alpha, IL-1beta, and IL-6. Production of these cytokines was followed by the expression of matrix metalloproteinases (MMPs) 1 and 3, which could be involved in the articular damage that has been observed in disease induced by SinV. The use of different strategies to block MIF action, including an anti-MIF antibody, the MIF inhibitor ISO-1 and knockout mice for the MIF gene, showed that cytokine secretion and MMP expression during infection were regulated by MIF, suggesting that this cytokine acts in autocrine and paracrine manner upstream in the macrophage activation cascade. Thus, these are remarkable similarities between macrophage responses induced by SinV infection and those observed in rheumatoid arthritis, despite the different etiologies of infectious and autoimmune arthritides.

show abstract

Section: Remarkable Similarities Between Macrophage Responses In Sinvmentioning

confidence: 46%

Pro‐inflammatory response resulting from sindbis virus infection of human macrophages: Implications for the pathogenesis of viral arthritis

Assunção‐Miranda

Bozza

Poian

2009

Journal of Medical Virology

View full text Add to dashboard Cite

show abstract

“…Although the potential impact of IL-10 on the pathogenesis of RA has been under intensive study, its exact image is still vague (Brennan and Beech 2007;Firestein 2003;McInnes and Schett 2007). This anti-inflammatory cytokine is known to have an important regulatory effect on immunological and inflammatory reactions and to be a key factor in resolving chronic inflammation (Ouyang et al 2011;van Roon et al 2001), and to reduce the production of proinflammatory cytokines such as interleukin-1 13 (IL-1), TNF-α, and interleukin 2 (IL-2) (Liu et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Effect of galantamine on adjuvant-induced arthritis in rats

Gowayed

Refaat

Ahmed

et al. 2015

European Journal of Pharmacology

View full text Add to dashboard Cite

“…Hence, we examined the expression levels of the p40 common chain that is shared by the Th1-promoting cytokine IL-12 and the Th17-promoting cytokine IL-23 (9, 13, 31). Expression of p40 was shown to be critical in the pathogenesis of organ-specific autoimmune disorders, particularly multiple sclerosis (10) and chronic inflammatory arthritis (31,32). Analysis of p40 expression in MLNs and ILNs at day 21 postinfection revealed critical differences in TNFRp55 2/2 mice versus WT mice (Fig.…”

Section: Tnfr P55 Signaling Regulates P40 Expression In Mlns and Ilnsmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Update on cytokines in rheumatoid arthritis

Cited by 75 publications

References 51 publications

Pro‐inflammatory response resulting from sindbis virus infection of human macrophages: Implications for the pathogenesis of viral arthritis

Pro‐inflammatory response resulting from sindbis virus infection of human macrophages: Implications for the pathogenesis of viral arthritis

Effect of galantamine on adjuvant-induced arthritis in rats

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

Contact Info

Product

Resources

About