The effect of treatment with interferon-gamma on type II collagen-induced arthritis

Nakajima, Hiroshi; Takamori, Hideo; Hiyama, Yoshiyuki; Tsukada, Wataru

doi:10.1111/j.1365-2249.1990.tb05353.x

Cited by 86 publications

(18 citation statements)

References 15 publications

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“…An early study in CIA disease induced by injection with collagen type II in Incomplete Freund's Adjuvant (IFA) supplemented with Mycobacterium species antigens (Complete Freund's Adjuvant (CFA)) found that administration of IFNc to the site of auto-inflammation exacerbated disease [145] possibly by enhancing inflammatory cell recruitment to the site. If however IFNc was administered outside the inflammatory site it had an ameliorating effect suggested to work through modulation of auto-antibody production [146]. This second effect was similar to the results observed in IFNcR deficient systems that suggested IFNc had a generally anti-inflammatory effect apparently by inhibiting signaling through IL-17 [147][148][149][150].…”

Section: Rheumatoid Arthritis (Ra)supporting

confidence: 71%

“…In these studies the anti-inflammatory effects of IFNc are thought to be related to modulation of the T cell differentiation program necessary to drive pathology or modulation of tissue activities, such as chemokine production, that in turn modulate immune cell recruitment. In contrast, in both studies of EAE and CIA introduction of IFNc at the site of ongoing inflammation resulted in exacerbated disease suggesting that IFNc is pro-inflammatory once fulminant inflammation is achieved [127,134,145,146].…”

Section: Discussionmentioning

confidence: 70%

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Interferon gamma in autoimmunity: A complicated player on a complex stage

Lees

2015

Cytokine

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Early views of autoimmune disease cast IFNγ as a prototypic pro-inflammatory factor. It is now clear that IFNγ is capable of both pro- and anti-inflammatory activities with the functional outcome dependent on the physiological and pathological setting examined. Here, the major immune modulatory activities of IFNγ are reviewed and current evidence for the impact of IFNγ on pathology and regulation of several autoimmune diseases and disease models is summarized.

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Section: Rheumatoid Arthritis (Ra)supporting

confidence: 71%

Section: Discussionmentioning

confidence: 70%

Interferon gamma in autoimmunity: A complicated player on a complex stage

Lees

2015

Cytokine

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“…Yet, in several studies, IFN-g was protective in CIA. We and others showed this by administering IFN-g or a neutralizing anti-IFN-g Ab or using genetically engineered mice with defective IFN-g production or action (56)(57)(58)(59)(60). IFN-g could exert its protective effect in CIA by inhibiting the differentiation of monocytes/macrophages into osteoclasts (61) and by inducing regulatory B10 cells in CIA (62).…”

Section: Discussionmentioning

confidence: 99%

In Vivo Expansion of Activated Foxp3+ Regulatory T Cells and Establishment of a Type 2 Immune Response upon IL-33 Treatment Protect against Experimental Arthritis

Biton

Athari

Thiolat

et al. 2016

The Journal of Immunology

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IL-33 is strongly involved in several inflammatory and autoimmune disorders with both pro- and anti-inflammatory properties. However, its contribution to chronic autoimmune inflammation, such as rheumatoid arthritis, is ill defined and probably requires tight regulation. In this study, we aimed at deciphering the complex role of IL-33 in a model of rheumatoid arthritis, namely, collagen-induced arthritis (CIA). We report that repeated injections of IL-33 during induction (early) and during development (late) of CIA strongly suppressed clinical and histological signs of arthritis. In contrast, a late IL-33 injection had no effect. The cellular mechanism involved in protection was related to an enhanced type 2 immune response, including the expansion of eosinophils, Th2 cells, and type 2 innate lymphoid cells, associated with an increase in type 2 cytokine levels in the serum of IL-33–treated mice. Moreover, our work strongly highlights the interplay between IL-33 and regulatory T cells (Tregs), demonstrated by the dramatic in vivo increase in Treg frequencies after IL-33 treatment of CIA. More importantly, Tregs from IL-33–treated mice displayed enhanced capacities to suppress IFN-γ production by effector T cells, suggesting that IL-33 not only favors Treg proliferation but also enhances their immunosuppressive properties. In concordance with these observations, we found that IL-33 induced the emergence of a CD39high Treg population in a ST2L-dependent manner. Our findings reveal a powerful anti-inflammatory mechanism by which IL-33 administration inhibits arthritis development.

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“…The role of IFN-␥ in CIA has since long been a subject of debate. Early attempts to identify its role by the administration of IFN-␥ or neutralizing anti-IFN-␥ mAb yielded conflicting results, probably because of variations in timing, sites, and means of administration (29,(52)(53)(54)(55). In two studies, anti-IFN-␥ Ab treatment caused an increase in the number of arthritic limbs or severity of arthritis (55,56), whereas in another study, the effect of anti-IFN-␥ depends on the time of administration, early treatment being associated with reduced severity and late treatment being associated with aggravation of the disease (29).…”

Section: Discussionmentioning

confidence: 99%

A Single Early Activation of Invariant NK T Cells Confers Long-Term Protection against Collagen-Induced Arthritis in a Ligand-Specific Manner

Coppieters

Beneden

Jacques

et al. 2007

The Journal of Immunology

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The glycosphingolipid α-galactosylceramide (α-GalCer) has been shown to be a potent activator of invariant NKT (iNKT) cells, rapidly inducing large amounts of both Th1 and Th2 cytokines upon injection in mice. The C-glycoside analog of α-GalCer (α-C-GalCer), by contrast, results in an enhanced Th1-type response upon activation of iNKT cells. We administered a single dose of these Ags to DBA/1 mice during the early induction phase of collagen-induced arthritis and demonstrated therapeutic efficacy of α-GalCer when administered early rather than late during the disease. Surprisingly, the Th1-polarizing analog α-C-GalCer also conferred protection. Furthermore, a biphasic role of IFN-γ in the effect of iNKT cell stimulation was observed. Whereas in vivo neutralization of IFN-γ release induced by either α-GalCer or α-C-GalCer early during the course of disease resulted in partial improvement of clinical arthritis symptoms, blockade of IFN-γ release later on resulted in a more rapid onset of arthritis. Although no phenotypic changes in conventional T cells, macrophages, or APCs could be detected, important functional differences in T cell cytokine production in serum were observed upon polyclonal T cell activation, 2 wk after onset of arthritis. Whereas α-GalCer-treated mice produced significantly higher amounts of IL-10 upon systemic anti-CD3 stimulation compared with PBS controls, T cells from α-C-GalCer-treated mice, by contrast, produced substantially lower levels of cytokines, suggesting the involvement of different protective mechanisms. In conclusion, these findings suggest long-term, ligand-specific, time-dependent, and partially IFN-γ-dependent immunomodulatory effects of iNKT cells in collagen-induced arthritis.

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The effect of treatment with interferon-gamma on type II collagen-induced arthritis

Cited by 86 publications

References 15 publications

Interferon gamma in autoimmunity: A complicated player on a complex stage

Interferon gamma in autoimmunity: A complicated player on a complex stage

In Vivo Expansion of Activated Foxp3+ Regulatory T Cells and Establishment of a Type 2 Immune Response upon IL-33 Treatment Protect against Experimental Arthritis

A Single Early Activation of Invariant NK T Cells Confers Long-Term Protection against Collagen-Induced Arthritis in a Ligand-Specific Manner

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