2010
DOI: 10.1002/ibd.21167
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Targeting TGF-β1 by employing a vaccine ameliorates fibrosis in a mouse model of chronic colitis

Abstract: This TGF-beta1 peptide-based vaccine, which suppressed excessive TGF-beta1 bioactivity, may prevent the development of intestinal fibrosis and associated complications, presenting a novel approach in the treatment of IBD.

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Cited by 49 publications
(29 citation statements)
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“…2,3 Therefore, the control of TGF-b1 production has been investigated as a therapy for preventing and suppressing intestinal fibrosis. We read the great interest the published article by Ma et al 4 entitled ''Targeting TGF-b1 by employing a vaccine ameliorates fibrosis in a mouse model of chronic colitis.'' The authors demonstrated that this TGF-b1 peptide-based vaccine significantly reduced colonic collagen deposition in 2,4,6-trinitrobenzene sulfonic acid-induced chronic colitis.…”
Section: Heat Shock Protein 47 Can Be a New Target Molecule For Intesmentioning
confidence: 96%
“…2,3 Therefore, the control of TGF-b1 production has been investigated as a therapy for preventing and suppressing intestinal fibrosis. We read the great interest the published article by Ma et al 4 entitled ''Targeting TGF-b1 by employing a vaccine ameliorates fibrosis in a mouse model of chronic colitis.'' The authors demonstrated that this TGF-b1 peptide-based vaccine significantly reduced colonic collagen deposition in 2,4,6-trinitrobenzene sulfonic acid-induced chronic colitis.…”
Section: Heat Shock Protein 47 Can Be a New Target Molecule For Intesmentioning
confidence: 96%
“…Most of them have not been evaluated in animal models of intestinal fibrosis, a challenging enterprise that should yield relevant information on both mechanisms and efficacy. A different approach to anti-TGF-␤ therapy has been the use of a TGF-␤1 peptide-based virus-like particle vaccine (77). When tested in mice with TNBS-induced chronic colitis, inflammation and collagen deposition improved together with decreased Smad3 phosphorylation and other inflammatory markers.…”
Section: Relevance Of Animal Models To Human Intestinal Fibrosismentioning
confidence: 99%
“…23 Several peptide epitopes from inflammatory cytokines which are key mediators in pathogenesis of asthma or inflammatory bowel diseases have been successfully presented onto the surface of HBcAg VLPs, and immunization with these VLPs ameliorated significantly the development of diseases manifests in animal models. 13,[24][25][26] However, linear epitopes may be not powerful enough to elicit efficient neutralizing antibodies (our unpublished data). Moreover, based on our previous experience, the assembling ability of HBcAg might be destroyed even if a short peptide is inserted, and sometimes even an amino acid alteration within the successfully inserted peptide would hamper the VLPs assembly (our unpublished data).…”
Section: Discussionmentioning
confidence: 96%