Collagen II-pulsed antigen-presenting cells genetically modified to secrete IL-4 down-regulate collagen-induced arthritis

Guéry, Laurence; Chiocchia, Gilles; Batteux, Frédéric; Mc, Boissier; Fournier, Catherine

doi:10.1038/sj.gt.3301613

Cited by 22 publications

(13 citation statements)

References 39 publications

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“…Because we attributed this failure to confer protection to cotransfer of IL-4-producing B cells (Fig. 8), it would explain the discrepancy with B cell transfer protecting in the collagen-induced arthritis (26), because in this model IL-4 is protective; treatment of mice with engineered IL-4-producing B cells (51) or IL-4-expressing dendritic cells (52) was shown to reduce or suppress arthritis.…”

Section: Discussionmentioning

confidence: 99%

Helminth Infection Protects Mice from Anaphylaxis via IL-10-Producing B Cells

Mangan

Fallon

Smith³

et al. 2004

The Journal of Immunology

248

208

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Modulation of the immune system by infection with helminth parasites, including schistosomes, is proposed to reduce the levels of allergic responses in infected individuals. In this study we investigated whether experimental infection with Schistosoma mansoni could alter the susceptibility of mice to an extreme allergic response, anaphylaxis. We formally demonstrate that S. mansoni infection protects mice from an experimental model of systemic fatal anaphylaxis. The worm stage of infection is shown to mediate this protective effect. In vivo depletion studies demonstrated an imperative role for B cells and IL-10 in worm-mediated protection. Furthermore, worm infection of mice increases the frequency of IL-10-producing B cells compared with that in uninfected mice. However, transfer of B cells from worm-infected mice or in vitro worm-modulated B cells to sensitized recipients exacerbated anaphylaxis, which was attributed to the presence of elevated levels of IL-4-producing B cells. Worm-modulated, IL-10-producing B cells from IL-4-deficient, but not IL-5-, IL-9- or IL-13-deficient, mice conferred complete resistance to anaphylaxis when transferred to naive mice. Therefore, we have dissected a novel immunomodulatory mechanism induced by S. mansoni worms that is dependent on an IL-10-producing B cell population that can protect against allergic hypersensitivity. These data support a role for helminth immune modulation in the hygiene hypothesis and further illustrate the delicate balance between parasite induction of protective regulatory (IL-10) responses and detrimental (IL-4) allergic responses.

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Section: Discussionmentioning

confidence: 99%

Helminth Infection Protects Mice from Anaphylaxis via IL-10-Producing B Cells

Mangan

Fallon

Smith³

et al. 2004

The Journal of Immunology

248

208

View full text Add to dashboard Cite

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“…The protective effect of IL-4 is improved in combination with IL-10 [142,143]. Additionally, DCs or APCs genetically engineered to over-express IL-4 are also able to suppress CIA and/or IL-17 production [144][145][146][147]. Administration of IL-4 during PGIA is also able to reduce disease [148].…”

Section: T H 2 Cells 261 Interleukin-4mentioning

confidence: 99%

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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“…62 T cells have also been targeted by DNA immunization against TCR idiotypes, 71 and blocking costimulatory molecules such as B7.1 and B7.2 using soluble CTLA-4-Ig 72 from an adenovirus injected intravenously. IL-4 was expressed in APCs (ie B cells and macrophages) pulsed with collagen type II 73 and also in a nonantigen-specific manner in dendritic cells 11 both with therapeutic results.…”

Section: T Cells and Their Function As Targetsmentioning

confidence: 99%