死の甘いキス：ガレクチン‐１，糖鎖修飾，免疫特権生成をつなぐもの

DOI Web Site 参考文献76件
  • Rubinstein Natalia
    División de Inmunogenética, Hospital de Clínicas “José de San Martin” Facultad de Medicina, Universidad de Buenos Aires
  • Toscano Marta A.
    División de Inmunogenética, Hospital de Clínicas “José de San Martin” Facultad de Medicina, Universidad de Buenos Aires
  • Ilarregui Juan M.
    División de Inmunogenética, Hospital de Clínicas “José de San Martin” Facultad de Medicina, Universidad de Buenos Aires
  • Bianco Germán A.
    División de Inmunogenética, Hospital de Clínicas “José de San Martin” Facultad de Medicina, Universidad de Buenos Aires
  • Rabinovich Gabriel A.
    Laboratorio de Inmunogenética. Hospital de Clínicas “José de San Martín”
  • 佐々木 洋子
    帝京大学薬学部 生物化学教室

書誌事項

タイトル別名
  • The Sweet Kiss of Death: A Link between Galectin-1, Glycosylation and the Generation of Immune Privilege
  • シ ノ アマイ キス ガレクチン 1 トウサ シュウショク メンエキ トッケン セイセイ オ ツナグ モノ ガン エイゴ ゲンブン
  • A Link between Galectin-1, Glycosylation and the Generation of Immune Privilege
  • ガレクチン-1、糖鎖修飾、免疫特権生成をつなぐもの

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説明

Galectin-1 (Gal-1), a member of a family of highly conserved carbohydrate-binding proteins, has been reported to be a potent immunosuppressive and anti-inflammatory factor. It has been proposed that the presence of galectin-1 in organs such as the eye, the placenta, reproductive organs (testis, ovaries) and also in tumours might confer a status of immune privilege to these vulnerable sites. Up-regulated expression of this protein may contribute to preserve an immunosuppressive microenvironment by inducing apoptosis of inflammatory and effector T cells and skewing the balance of the local immune response towards a Th2 cytokine profile. Different glycosyltransferase enzymes are involved in the generation of specific saccharide ligands required for Gal-1 binding and Gal-1-induced cell death. Interestingly, expression of these enzymes is highly regulated during T cell development, activation and apoptosis. The aim of this review is to explore the potential link between glycosylation of immune cell subsets, susceptibility to Gal-1 and the generation of immune privilege, particularly in the context of tumor-immune escape.

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