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Mϕs promote tissue injury or repair depending on their activation status and the local cytokine milieu. It remains unclear whether the immunosuppressive effects of transforming growth factor β (TGF-β) serve a nonredundant role in Mϕ function in vivo. We generated Mϕ-specific transgenic mice that express a truncated TGF-β receptor II under control of the CD68 promoter (CD68TGF-βDNRII) and subjected these mice to the dextran sodium sulfate (DSS) model of colitis. CD68TGF-βDNRII mice have an impaired ability to resolve colitic inflammation as demonstrated by increased lethality, granulocytic inflammation, and delayed goblet cell regeneration compared with transgene negative littermates. CD68TGF-βDNRII mice produce significantly less IL-10, but have increased levels of IgE and numbers of IL-33+ Mϕs than controls. These data are consistent with associations between ulcerative colitis and increased IL-33 production in humans and suggest that TGF-β may promote the suppression of intestinal inflammation, at least in part, through direct effects on Mϕ function.

Original publication

DOI

10.1002/eji.201041135

Type

Journal article

Journal

Eur J Immunol

Publication Date

07/2011

Volume

41

Pages

2000 - 2009

Keywords

Animals, Antigens, CD, Antigens, Differentiation, Myelomonocytic, Blotting, Southern, Colitis, Colitis, Ulcerative, Dextran Sulfate, Disease Models, Animal, Flow Cytometry, Immunoglobulin E, Interleukin-33, Interleukins, Macrophages, Mice, Mice, Transgenic, Promoter Regions, Genetic, Receptors, Transforming Growth Factor beta, Transforming Growth Factor beta