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      Cryptosporidium parvum induces B7-H1 expression in cholangiocytes by down-regulating microRNA-513.

      The Journal of Infectious Diseases
      Antigens, CD, metabolism, Antigens, CD274, Apoptosis, Bile Ducts, cytology, parasitology, Cells, Cultured, Coculture Techniques, Cryptosporidium parvum, pathogenicity, Down-Regulation, Epithelial Cells, Humans, MicroRNAs, T-Lymphocytes

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          Abstract

          Expression of B7 costimulatory molecules represents an important compartment of immune response of epithelial cells after microbial infection. We report here that the protozoan parasite Cryptosporidium parvum induced B7-H1 expression in cultured human cholangiocytes. Induced expression of B7-H1 was identified in cells after exposure to infective C. parvum parasite or parasite lysate. Interestingly, the level of microRNA-513 (miR-513) was reduced in cells after exposure to C. parvum, which resulted in a relief of 3' untranslated region-mediated translational suppression of B7-H1. Overexpression of miR-513 through transfection of miR-513 precursor inhibited C. parvum-induced B7-H1 protein expression. Moreover, enhanced apoptotic cell death was identified in activated human T cells after coculture with C. parvum-infected cholangiocytes. The apoptosis of activated T cells was partially blocked by a neutralizing antibody to B7-H1 or transfection of cholangiocytes with miR-513 precursor. These data suggest a role of miR-513 in regulating B7-H1 expression by cholangiocytes in response to C. parvum infection.

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