Chronic relapsing homologous collagen‐induced arthritis in DBA/1 mice as a model for testing disease‐modifying and remission‐inducing therapies

Malfait, Anne-Marie; Williams, Richard O.; Malik, Angela Sara; Maini, R. N.; Feldmann, Marc

doi:10.1002/1529-0131(200105)44:5<1215::aid-anr206>3.0.co;2-#

Cited by 46 publications

(25 citation statements)

References 31 publications

(38 reference statements)

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“…By modulating effector function of memory T cells, PGE2 would enhance IL-17 production even in the presence of effector cells capable of producing IFN-g, providing a mechanism to explain why Th17 responses prevail in chronic inflammation sites, despite the presence of high numbers of Th1 cells. Moreover, the finding that PGE2 had a rapid effect on already differentiated effector T cells is in line with the fact that treatment with nonsteroidal anti-inflammatory drugs (NSAID) is effective shortly after administration even when the disease is already established, and that it is able to relieve the symptoms but does not prevent disease progression [55]. Interestingly, PGE2 was able to increase IL-17 but inhibited IL-22, a cytokine that is also produced by Th17 cells and has been implicated in skin inflammatory processes such as psoriasis [56].…”

Section: Discussionmentioning

confidence: 70%

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4⁺ T cells

Napolitani¹,

et al. 2009

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The contribution of Th1 and Th17 cells in chronic inflammatory conditions leading to autoimmunity remains highly controversial. In inflamed tissues, production of prostaglandins by COX-2 has been proposed to favor Th17 responses indirectly by increasing IL-23 and blocking IL-12 release from APC. We report here that prostaglandin E2 (PGE2) can directly modulate cytokine production by human memory CD4 1 T cells. TCR triggering in the presence of PGE2 increased IL-17 and reduced IFN-c production by freshly isolated memory T cells or T-cell clones. PGE2 triggered the EP2 and EP4 receptors expressed on T cells leading to a rapid increase of retinoic-acid-related orphan receptor-ct (ROR-ct) and decrease of T-cell-specific T-box transcription factor 21 (T-bet) mRNA. Moreover, PGE2 promoted the selective enrichment of IL-17-producing cells by differentially modulating the proliferation of memory T-cell subsets in vitro. Taken together our results indicate that T-cell effector function is a direct target for PGE2 modulation and suggest a novel mechanism by which inhibitors of prostaglandin synthesis, such as COX-2 inhibitors, exert their anti-inflammatory effect.Key words: IFN-c . IL-17 . Memory T cells . Prostaglandin . Th17Supporting Information available online IntroductionIL-17-producing T cells (Th17) have been recently characterized as a distinct lineage of CD4 + Th cells. IL-17 and Th17 cells have been shown to mediate protection against extracellular pathogens by promoting neutrophil recruitment [1][2][3][4] but also to cause immunopathology in different models of autoimmunity [5]. Differentiation of mouse Th17 cells from uncommitted naïve T-cell precursors is controlled by the lineage-specific transcription factors retinoic-acid-related orphan receptor-gt (ROR-gt) [6] and , is promoted by an IL-21-autocrine loop triggered by 9] and inhibited by Th1-or Th2-promoting stimuli, such as IL-12, IFN-g and IL-4. Human Th17 cell differentiation is associated with increased expression of ROR-g, is induced by IL-1b and enhanced by 11] while requirement for TGF-b is still debated and may be different depending on experimental conditions [12][13][14]. Both in vitrodifferentiated human and mouse Th17 cells selectively upregulate expression of the chemokine receptor CCR6 [15,16]. CCR6 is also expressed on circulating human memory Th17 cells and it has been shown to mediate recruitment of pathogenic Th17 cells in a mouse arthritis model [16]. The notion that Th17 cells are implicated in the onset and maintenance of autoimmune diseases is supported by compelling evidence. In mice, transfer of Th17 but not Th1 cells induce EAE Before identification of Th17 cells, Th1 cells and the Th1-associated cytokine IFN-g were thought to play a pathogenic role in autoimmune diseases [29]. However, the findings that IFN-gand IFN-R-deficient mice had higher susceptibility to EAE and CIA compared with wild-type mice [30][31][32] and that administration of neutralizing antibodies to IFN-g exacerbated MS in human patients [33] were pointing to an...

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Section: Discussionmentioning

confidence: 70%

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4⁺ T cells

Napolitani¹,

et al. 2009

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“…In contrast, RA in humans is a chronic, progressive condition that more closely resembles the chronic disease induced in mice using autologous type II collagen. It is interesting to note that, in common with human RA, NSAIDs do not act as DMARDs in this chronic CIA model (38). Such differences in human RA and heterologous CIA may also be reflected in the cellular composition of synovial cell membrane preparations.…”

Section: Discussionmentioning

confidence: 92%

Nonsteroidal Anti-Inflammatory Drugs Increase TNF Production in Rheumatoid Synovial Membrane Cultures and Whole Blood

Page

Turner

Brown

et al. 2010

The Journal of Immunology

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“…It has been shown that prednisolone given for an extended period is capable of ameliorating joint damage in both collagen- (Paska et al, 1986;Geiger et al, 1994) and antigen-induced (van den Berg et al, 1991) murine arthritis. Conversely, it has been shown that in these same models, indomethacin does not reverse pathological changes in the joint, even following long-term treatment (de Vries et al, 1988;Cannon et al, 1990;Malfait et al, 2001). Further work will be required to determine if long-term steroid administration can significantly reduce the pathological changes associated with FCA-induced arthritis.…”

Section: Discussionmentioning

confidence: 96%

A robust model of adjuvant-induced chronic unilateral arthritis in two mouse strains

Gauldie

McQueen

Clarke

et al. 2004

Journal of Neuroscience Methods

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Chronic relapsing homologous collagen‐induced arthritis in DBA/1 mice as a model for testing disease‐modifying and remission‐inducing therapies

Cited by 46 publications

References 31 publications

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4⁺ T cells

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4⁺ T cells

Nonsteroidal Anti-Inflammatory Drugs Increase TNF Production in Rheumatoid Synovial Membrane Cultures and Whole Blood

A robust model of adjuvant-induced chronic unilateral arthritis in two mouse strains

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Chronic relapsing homologous collagen‐induced arthritis in DBA/1 mice as a model for testing disease‐modifying and remission‐inducing therapies

Cited by 46 publications

References 31 publications

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4+ T cells

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4+ T cells

Nonsteroidal Anti-Inflammatory Drugs Increase TNF Production in Rheumatoid Synovial Membrane Cultures and Whole Blood

A robust model of adjuvant-induced chronic unilateral arthritis in two mouse strains

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Product

Resources

About

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4⁺ T cells

Prostaglandin E2 enhances Th17 responses via modulation of IL‐17 and IFN‐γ production by memory CD4⁺ T cells