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Autocrine Regulation of T Cell Motility by Calreticulin-Thrombospondin-1 Interaction¹

Shu Shun Li^*,, Anna Forslöw^*, and Karl-Gösta Sundqvist^2,*,

^* Division of Clinical Immunology, Department of Clinical Microbiology, Umeå University, Umeå, Sweden; and Division of Clinical Immunology, Department of Laboratory Medicine, Karolinska University Hospital, Stockholm, Sweden

The mechanisms regulating T lymphocyte migration within the extracellular matrix are not understood. We show in this study that the thrombospondin-1 binding site of calreticulin, spanning aa 19–32, is a major triggering factor for T cell motility and migration within a three-dimensional collagen type 1 matrix, and that exogenous motogenic factors such as chemokines can stimulate migration via a calreticulin-thrombospondin-1 pathway. Endogenous calreticulin binding to the N-terminal domain of endogenous thrombospondin-1 elicited a motogenic signal to the T cells through the C-terminal domain of thrombospondin-1 and its cell surface receptor integrin-associated protein (CD47). Our data further revealed that thrombospondin-1 was expressed on the cell surface with a high turnover, and that PI3K and the Janus family of tyrosine kinases were required for T cell motility mediated through calreticulin, thrombospondin-1, and CD47. These results unveil an autocrine mechanism of calreticulin-thrombospondin-1-CD47 interaction for the control of T cell motility and migration within three-dimensional extracellular matrix substrata.

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