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BAMBI inhibition protects mice against the development of Dextran Sodium Sulphate-induced colitis

AutorMuñoz, Marta; Gil, Thais M.; Álvarez, Pilar; Merino, Jesús; Merino, Ramón
Fecha de publicación2017
EditorSociedad Española de Inmunología
Citación40 Congreso de la Sociedad Española de Inmunología (2017)
Resumen[Introduction]: BAMBI (BMP and Activin membrane bound inhibitor) is a transmembrane protein similar to TGFß type I receptors that antagonizes TGFß family signals. Recently, we have demonstrated that BAMBI is induced after activation of CD4 T cells and controls their functional differentiation into CD4 regulatory T (Tregs) and TH17 cells. Accordingly, BAMBI deficient mice (BAMBI-KO) are protected against the development of autoimmune arthritis by mechanisms dependent on Tregs and TGFß. [Objectives]: In the present study we have explored the role of BAMBI in the development of dextran sulphate-induced colitis (DSS-colitis), a well stablished model of inflammatory bowel disease. [Methods]: DSS-colitis was induced in BAMBI-KO and B6 wild type (WT) mice treated or not with 2 mg/week of B101.37, an anti-BAMBI monoclonal antibody developed recently in our laboratory. [Results]: A significantly reduced severity of DSS-colitis is observed in both BAMBI-KO and B101.37-treated B6 WT mice. Such protection is mediated by TGFß but not by other growth factors of the TGFß superfamily that are also regulated by BAMBI. In vivo Treg depletion experiments with anti-CD25 mAbs and the analysis bone marrow chimeric mice reveal that immune regulatory-mediated mechanisms are not involved in the protection against DSS-colitis observed in B6.BAMBI-KO mice, unlike that observed in autoimmune arthritis. Instead, the gut epithelium from these mutant mice shows a reduced permeability after DSS exposure. [Conclusions]: Our study points to BAMBI as a regulator of gut epithelium permeability controlling in that way the susceptibility of mice to inflammatory bowel diseases.
DescripciónResumen del póster presentado al 40 Congreso de la Sociedad Española de Inmunología, celebrado en Zaragoza del 25 al 27 de mayo de 2017.
URIhttp://hdl.handle.net/10261/164847
Aparece en las colecciones: (IBBTEC) Comunicaciones congresos
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