Effect of a monoclonal antibody against interleukin‐4 on collagen‐induced arthritis in mice

Yoshino, Shigefumi

doi:10.1038/sj.bjp.0701607

Cited by 24 publications

(22 citation statements)

References 34 publications

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“…Similarly, in CIA, injections of anti-IL-4 i.p. for 10 days initiated on the day of immunization with type II articular cartilage collagen markedly augmented the incidence and severity of arthritis (25). However, anti-IL-4 Ab did not affect CIA incidence or macroscopic arthritis evaluation in a similar study (26).…”

Section: Discussionmentioning

confidence: 87%

IL-4 Adenoviral Gene Therapy Reduces Inflammation, Proinflammatory Cytokines, Vascularization, and Bony Destruction in Rat Adjuvant-Induced Arthritis

Woods¹,

Katschke²,

Volin³

et al. 2001

The Journal of Immunology

131

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IL-4 is a cytokine with anti-inflammatory properties on activated macrophages. Rheumatoid arthritis, an autoimmune inflammatory disease, is characterized by a paucity of IL-4 and an abundance of synovial macrophage-derived mediators. Herein, the effect of a single injection of adenovirus-producing rat IL-4 (AxCAIL-4) or a control virus with no inserted gene was compared with the effect of PBS injection into rat ankles. Ankles were injected before arthritis onset or at maximal inflammation. Preventatively, AxCAIL-4 reduced adjuvant-induced arthritis (AIA)- and/or AIA/adenoviral-induced ankle inflammation, decreasing articular index scores, ankle circumferences, paw volumes, radiographic scores, mean levels of monocyte chemoattractant protein-1, the number of inflammatory cells, and the number of synovial blood vessels. Therapeutically, AxCAIL-4 also decreased ankle circumferences and paw volumes in comparison with a control virus with no inserted gene and PBS groups. After arthritis onset, mean levels of TNF-α, IL-1β, macrophage inflammatory protein-2, and RANTES were decreased in AxCAIL-4 rat ankle homogenates compared with PBS-treated homogenates. Thus, increased expression of IL-4 via gene therapy administered in a preventative and/or therapeutic manner reduced joint inflammation, synovial cellularity, levels of proinflammatory cytokines, vascularization, and bony destruction in rat AIA, suggesting that a similar treatment in humans may be beneficial.

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Section: Discussionmentioning

confidence: 87%

IL-4 Adenoviral Gene Therapy Reduces Inflammation, Proinflammatory Cytokines, Vascularization, and Bony Destruction in Rat Adjuvant-Induced Arthritis

Woods¹,

Katschke²,

Volin³

et al. 2001

The Journal of Immunology

131

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“…Prophylactic treatment with IL-4 mAbs was able to significantly reduce the incidence and clinical score [151]. Interestingly, IL-4 À/À mice were only protected from CIA when immunised with collagen in incomplete Freund's adjuvant.…”

Section: T H 2 Cells 261 Interleukin-4mentioning

confidence: 93%

Effector T cells in rheumatoid arthritis: Lessons from animal models

Alzabin

Williams

2011

FEBS Letters

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The development of an immune response to self antigens drives naive T cells to differentiate into subsets of CD8+ and CD4+ effector cells including TH1, TH2, cells and the more recently described TH17, and regulatory T cells (Treg). Rheumatoid arthritis is an autoimmune disease that engages an uncontrolled influx of inflammatory cells to the joints, eventually leading to joint damage. The role that effector T cells play in the local or systemic maintenance of, or protection against, inflammation and subsequent joint damage is now becoming better understood through the use of animal models. In this review, we will explore the different animal models of RA, and their contribution to elucidating the role that effector T cells play in the regulation, induction, and maintenance of inflammatory joint disease. This understanding will aid in the design of more effective therapeutic strategies for rheumatoid arthritis and other autoimmune disorders.

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“…Th1 cells, which produce interferon-(IFN-), have been considered to be the major player in CIA. In fact, spleen cells from CIA mice produce a large amount of IFN-after antigen stimulation in vitro [3]. Recently, interleukin-17 (IL-17)-producing Th17 cells have been identiWed, and recent studies have suggested that Th17 cells play a central role in the pathogenesis of autoimmune disease, because neutralization or genetic deletion of IL-17 inhibits the development of disease in several autoimmune disease models including CIA model [4,5].…”

Section: Introductionmentioning

confidence: 99%

IL-6 blockade preferentially inhibits Th17 differentiation in collagen-induced arthritis

Yoshida¹,

Hashizume²,

Mihara³

2010

Rheumatol Int

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We examined the time course of cytokine production by CD4 T cells from mice with collagen-induced arthritis (CIA), and we determined the influence of interleukin-6 (IL-6) blockade on cytokine production. CD4 T cells purified from spleen were cultured with both collagen and anti-CD28 antibody for 48 h and the production of interferon-γ (IFN-γ), IL-4, and IL-17 by the cells, secreted into the supernatants, was measured at various time intervals. The production of all these cytokines started 7 days after the first immunization. A marked increase in IFN-γ production was observed after the second immunization, but IL-4 and IL-17 production was not affected by a second immunization. A single injection of anti-mouse IL-6 receptor antibody (MR16-1) on the day of the first immunization suppressed the onset of arthritis. IL-17 production by CD4 T cells from MR16-1-treated mice was significantly lower than that from the control mice. On the other hand, treatment with MR16-1 showed only a tendency to suppress the production of IL-4 and IFN-γ. Injection of MR16-1 on day 21 did not suppress the onset of arthritis. We examined the direct influence of MR16-1 on cytokine production by differentiated CD4 T cells from arthritic mice. Production of IL-4, IFN-γ, and IL-17 was not affected by MR16-1. In conclusion, IL-6 inhibition preferentially suppresses the induction of Th17 cells and does not seem to impact on cytokine production of already differentiated Th17 cells.

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Effect of a monoclonal antibody against interleukin‐4 on collagen‐induced arthritis in mice

Cited by 24 publications

References 34 publications

IL-4 Adenoviral Gene Therapy Reduces Inflammation, Proinflammatory Cytokines, Vascularization, and Bony Destruction in Rat Adjuvant-Induced Arthritis

IL-4 Adenoviral Gene Therapy Reduces Inflammation, Proinflammatory Cytokines, Vascularization, and Bony Destruction in Rat Adjuvant-Induced Arthritis

Effector T cells in rheumatoid arthritis: Lessons from animal models

IL-6 blockade preferentially inhibits Th17 differentiation in collagen-induced arthritis

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