Involvement of αEβ7 (CD103) in the pathogenesis of autoimmune diseases

Keiko Yoshimoto, Takahiko Kurasawa, Katsuya Suzuki, Tsutomu Takeuchi

研究成果: Article査読

1 被引用数 (Scopus)


αEβ7 (CD103), one of integrin family molecules, is a heterodimer consisting of an αE subunit and a β7 subunit. αEβ7 is expressed in several subsets of lymphocytes including T cells, intestinal intraepithelial lymphocytes and lamina propria lymphocytes. αEβ7 a ligand for E-cadherin, which is mainly expressed in epithelial cells, and an interaction between αEβ7 and E-cadherin results in adhesion of lymphocytes to epithelial cells. We found that EC5 domain, one of domains consisting E-cadherin, was indispensable for binding of E-cadherin with αEβ7. Accumulating evidence suggests that αEβ7 is not only involved in intestinal immune responses but also tissue damages associated with inflammatory diseases including autoimmune diseases. While E-cadherin is constitutively expressed in epithelial cells, the expression of αEβ7 is induced in T cells upon inflammatory stimulation in vitro. In addition, TGF-β1 induces the expression of αEβ7 via a pathway including Smad. These findings raise the possibility that αEβ7 is a potential therapeutic target for inflammatory diseases. We postulate that molecules that interfere with interaction between αEβ7 and E-cadherin are drug candidates for the diseases. We have been focusing on αEβ7 and vigorously investigating the mechanism that underlies the pathogenesis of autoimmune diseases.

ジャーナルJapanese Journal of Clinical Immunology
出版ステータスPublished - 2014

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学


「Involvement of αEβ7 (CD103) in the pathogenesis of autoimmune diseases」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。