論文

国際誌
2011年12月15日

Molecular cloning of bovine lymphocyte activation gene-3 and its expression characteristics in bovine leukemia virus-infected cattle.

Veterinary immunology and immunopathology
  • Tatsuya Shirai
  • ,
  • Satoru Konnai
  • ,
  • Ryoyo Ikebuchi
  • ,
  • Tomohiro Okagawa
  • ,
  • Saori Suzuki
  • ,
  • Yuji Sunden
  • ,
  • Misao Onuma
  • ,
  • Shiro Murata
  • ,
  • Kazuhiko Ohashi

144
3-4
開始ページ
462
終了ページ
7
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.vetimm.2011.08.018

Lymphocyte activation gene-3 (LAG-3), a major histocompatibility complex (MHC) class II binding CD4 homologue has recently been shown as one of the mechanisms for down-regulating immune responses during chronic disease progression. For the first time, we cloned LAG-3 from two breeds of cattle (Holstein and Japanese Black), and analyzed its expression levels in cattle infected with bovine leukemia virus (BLV), a chronic viral infection that leads to immuno-suppression. The cloned cDNA of bovine LAG-3 have an open reading frame of 1551 nucleotides, encoding a polypeptide of 515 amino acids in length. Similar to the swine LAG-3, the bovine LAG-3 protein sequence consisted of four extracellular domains, a transmembrane domain and an inhibitory motif, KTGELE. We found that the bovine LAG-3 mRNA transcripts were expressed predominantly on T-cells such as CD4(+) and CD8(+) cells, among peripheral blood mononuclear cells. In subsequent expression analysis, LAG-3 mRNA expression on CD4(+) T-cells from BLV-infected cattle was upregulated compared to that in normal cattle. Comparable results were obtained with CD8(+) T-cells from cattle infected with BLV. We further observed strong upregualtion of MHC class II molecule, the ligand for LAG-3 in BLV-infected cattle. These findings indicate an important role for inhibitory receptor molecules such as LAG-3 in chronic bovine infections and future studies will elucidate the specific role of LAG-3 in bovine diseases.

リンク情報
DOI
https://doi.org/10.1016/j.vetimm.2011.08.018
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21981995
ID情報
  • DOI : 10.1016/j.vetimm.2011.08.018
  • PubMed ID : 21981995

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