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Altered expression of Butyrophilin (BTN) and BTN-like (BTNL) genes in intestinal inflammation and colon cancer

Artikel i vetenskaplig tidskrift
Författare Cristina Lebrero-Fernandez
Ulf Alexander Wenzel
Paulina Akeus
Ying Wang
Hans Strid
Magnus Simrén
Bengt Gustavsson
Lars Börjesson
Susanna Cardell
Lena Öhman
Marianne Quiding-Järbrink
Anna Bas-Forsberg
Publicerad i Immunity Inflammation and Disease
Volym 4
Nummer/häfte 2
Sidor 191-200
ISSN 2050-4527
Publiceringsår 2016
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för kirurgi
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Sidor 191-200
Språk en
Länkar dx.doi.org/10.1002/iid3.105
Ämnesord Butyrophilin (Btn)-like (Btnl), colon cancer, immune regulation, intestinal inflammation, irritable bowel syndrome (IBS), ulcerative colitis (UC), delta t-cells, ulcerative-colitis, ovarian-cancer, activation, molecule, variants, susceptibility, stimulation, recognition, association, Immunology
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

Several Butyrophilin (BTN) and Btn-like (BTNL) molecules control T lymphocyte responses, and are genetically associated with inflammatory disorders and cancer. In this study, we present a comprehensive expression analysis of human and murine BTN and BTNL genes in conditions associated with intestinal inflammation and cancer. Using real-time PCR, expression of human BTN and BTNL genes was analyzed in samples from patients with ulcerative colitis, irritable bowel syndrome, and colon tumors. Expression of murine Btn and Btnl genes was examined in mouse models of spontaneous colitis (Muc2(-/-)) and intestinal tumorigenesis (Apc(Min/+)). Our analysis indicates a strong association of several of the human genes with ulcerative colitis and colon cancer; while especially BTN1A1, BTN2A2, BTN3A3, and BTNL8 were significantly altered in inflammation, colonic tumors exhibited significantly decreased levels of BTNL2, BTNL3, BTNL8, and BTNL9 as compared to unaffected tissue. Colonic inflammation in Muc2(-/-) mice significantly down-regulated the expression of particularly Btnl1, Btnl4, and Btnl6 mRNA, and intestinal polyps derived from Apc(Min/+) mice displayed altered levels of Btn1a1, Btn2a2, and Btnl1 transcripts. Thus, our data present an association of BTN and BTNL genes with intestinal inflammation and cancer and represent a valuable resource for further studies of this gene family.

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