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Butyrophilin-like 1 encodes an enterocyte protein that selectively regulates functional interactions with T lymphocytes.

Review article
Authors Anna Bas
Mahima Swamy
Lucie Abeler-Dörner
Gareth Williams
Dick J Pang
Susannah D Barbee
Adrian C Hayday
Published in Proceedings of the National Academy of Sciences of the United States of America
Volume 108
Issue 11
Pages 4376-81
ISSN 1091-6490
Publication year 2011
Published at Institute of Biomedicine
Pages 4376-81
Language en
Links dx.doi.org/10.1073/pnas.1010647108
Keywords Amino Acid Sequence, Animals, Cell Communication, Cytokines, metabolism, Enterocytes, metabolism, Epithelial Cells, cytology, metabolism, Gene Expression Regulation, Glycoproteins, chemistry, genetics, metabolism, HEK293 Cells, Humans, Intestine, Small, cytology, metabolism, Membrane Glycoproteins, chemistry, genetics, metabolism, Mice, Molecular Sequence Data, Protein Transport, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes, cytology, metabolism
Subject categories Microbiology in the medical area

Abstract

Although local regulation of T-cell responses by epithelial cells is increasingly viewed as important, few molecules mediating such regulation have been identified. Skint1, a recently identified member of the Ig-supergene family expressed by thymic epithelial cells and keratinocytes, specifies the murine epidermal intraepithelial lymphocyte (IEL) repertoire. Investigating whether Skint1-related molecules might regulate IEL in other compartments, this study focuses on buytrophilin-like 1 (Btnl1), which is conspicuously similar to Skint1 and primarily restricted to small intestinal epithelium. Btnl1 protein is mostly cytoplasmic, but surface expression can be induced, and in vivo Btnl1 can be detected adjacent to the IEL. In a newly developed culture system, enforced epithelial cell expression of Btnl1 attenuated the cells' response to activated IEL, as evidenced by suppression of IL-6 and other inflammatory mediators. These findings offer a unique perspective on emerging genetic data that Btnl genes may comprise novel and important local regulators of gut inflammation.

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