Expression of Fas ligand improves the effect of IL-4 in collagen-induced arthritis

Guéry, Laurence; Batteux, Frédéric; Bessis, Natacha; Bréban, Maxime; Boissier, Marie Christophe; Fournier, Catherine; Chiocchia, Gilles

doi:10.1002/1521-4141(200001)30:1<308::aid-immu308>3.0.co;2-x

Cited by 31 publications

(11 citation statements)

References 28 publications

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“…Recently, gene therapy approaches have also been extended to anti-inflammatory cytokines (ie IL-4 [197], IL-10 [182], IL-13 [104] and TGF-β [198]). An interesting approach of gene therapy is to achieve 'molecular synovectomy', either by expression of herpes simplex virus-thymidine kinase, with subsequent administration of ganciclovir [199,200], or by overexpression of Fas ligand, resulting in synovial cell apoptosis [201,202]. Gene therapy aimed at neutralizing proinflammatory macrophage products, overexpressing macrophage-regulating mediators, or simply eliminating overly activated macrophages therefore carries some promise for the treatment of arthritis [203].…”

Section: Experimental Antimacrophage Therapymentioning

confidence: 99%

Untitled

et al. 2000

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The abundance and activation of macrophages in the inflamed synovial membrane/pannus significantly correlates with the severity of rheumatoid arthritis (RA). Although unlikely to be the 'initiators' of RA (if not as antigen-presenting cells in early disease), macrophages possess widespread pro-inflammatory, destructive, and remodeling capabilities that can critically contribute to acute and chronic disease. Also, activation of the monocytic lineage is not locally restricted, but extends to systemic parts of the mononuclear phagocyte system. Thus, selective counteraction of macrophage activation remains as efficacious approach to diminish local and systemic inflammation, as well as to prevent irreversible joint damage. The electronic version of this article can be found online at http://arthritis-research.com/content/2/3/189 © Current Science Ltd AP = activator protein; BST = bone marrow stromal antigen; DMARD = disease-modifying antirheumatic drug; EBER(s) = Epstein-Barr virus-encoded small nuclear RNA(s); GM-CSF = granulocyte-macrophage colony-stimulating factor; GRO = growth-related oncogene protein; HLA = human leucocyte antigen; MCP = monocyte chemoattractant protein; MIP = macrophage inflammatory protein; NF-κB = nuclear factor-κB; NO = nitric oxide; RA = rheumatoid arthritis; TGF = transforming growth factor; Th = T-helper (cell); TIMP = tissue inhibitor of metalloproteinase; TNF = tumour necrosis factor.

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Section: Experimental Antimacrophage Therapymentioning

confidence: 99%

Untitled

et al. 2000

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“…Immunization with bovine native CII (100 mg emulsified in CFA, id), boosted with CII (100 mg in IFA) on day 121 and a blind evaluation of arthritis were performed as previously described in detail [14]. The date of disease onset was recorded, and the clinical severity of each joint or group of joints (toes, tarsus, ankle, wrist and knee) was graded: 0 (normal), 1 (erythema), 2 (swelling), 3 (deformity) or 4 (necrosis).…”

Section: Methodsmentioning

confidence: 99%

“…Conversely, several lines of evidence assign a protective role to Th-2 lymphocytes in CIA via production of anti-inflammatory cytokines. Thus, administration of Th-2-type cytokines such as IL-4, IL-10 and IL-13 are shown to reduce the incidence and the severity of clinical arthritis [11][12][13][14][15][16]. We and others have previously addressed the role of IFNg, a prototypic Th-1 type cytokine, in CIA.…”

Section: Introductionmentioning

confidence: 99%

Treatment of collagen‐induced arthritis by Natura‐α via regulation of Th‐1/Th‐17 responses

Glatigny

Blaton

Mencher³

et al. 2010

Eur J Immunol

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Cytokines and CD41 Th cells play a crucial role in the pathogenesis of rheumatoid arthritis. Among the Th populations, Th-1 and Th-17 have been described as pathogenic in collagen-induced arthritis (CIA) whereas Th-2 and Treg were found to have protective effects. The objective of this study was to examine the affect of Natura-a, a newly developed cytokine regulator, on CIA and on Th cell development. Natura-a treatment was administered before or during arthritis induction. Anti-type II collagen antibodies and cytokine expression were evaluated by ELISA. Emergence of CD4was assessed by flow cytometry. Th-17 differentiation of naive CD4 T cells was assessed in cultures with anti-CD3 and anti-CD28. We showed that Natura-a both prevented and treated CIA. We further demonstrated that in vivo treatment with Natura-a inhibited IL-17 production and anti-type II collagen IgG development. We showed in vitro, using an APCfree system, that Natura-a acted directly on differentiating T cells and inhibiting the formation of Th-1 and Th-17 cells but did not affect Th-2 cells. Since Natura-a inhibits a large spectrum of important pathogenic factors in CIA, it may provide a new and powerful approach to the treatment of rheumatoid arthritis and other inflammatory diseases.

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“…At present, combinations of different genes are being actively studied, because it would be difficult to treat the various pathological aspects of a disease with only one gene. 15,76,77 In the future, gene therapy could be prescribed in conjunction with other medication. Genes would be delivered to target tissues using an in vivo method and a nonviral vector, and the administration of various gene combinations could be selected at each stage of joint diseases.…”

Section: Future Prospectsmentioning

confidence: 99%