Effect of Tyrosine Kinase on TCR-Mediated Activation of Integrin

DOI
  • ITSUSAKI Hiroshi
    Department of Biochemistry, Osaka Dental University, Osaka, Japan
  • GODA Seiji
    Department of Biochemistry, Osaka Dental University, Osaka, Japan
  • KAMADA Aiko
    Department of Biochemistry, Osaka Dental University, Osaka, Japan
  • IKEO Takashi
    Department of Biochemistry, Osaka Dental University, Osaka, Japan

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Stimulation of the CD3/TCR results within minutes in an increase in T cell adhesion to fibronectin. The biochemical pathways that control TCR-mediated increases in adhesion to fibronectin remain poorly characterized. In this study, the role of the tyrosine kinase in the regulation of adhesion by the CD3/TCR was investigated. CD3 stimulation enhanced adhesion to fibronectin on Jurkat T cells line. Tyrosine kinase inhibitor, PP2, and anti β1 integrin mAb blocked adhesion to fibronectin enhanced by CD3 stimulation on Jurkat T cells. CD3 stimulation did not increase adhesion to fibronectin of the tyrosine kinase ZAP-70-deficient Jurkat T cells line, P116. Furthermore, CD3 stimulation failed to tyrosine phosphorylation of PI3-kinase enzyme AKT on P116 cells. These observations support a model in which the tyrosine kinase activity of ZAP-70 kinase is critical for regulation of β1 integrin activity by CD3/TCR.

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