NDLI: CD47 signaling regulates the immunosuppressive activity of VEGF in T cells *

Content Provider	PubMed Central
Author	Kaur, Sukhbir Chang, Tiffany Singh, Satya P. Lim, Langston Mannan, Poonam Garfield, Susan H. Pendrak, Michael L. Pantoja, David R. Soto Rosenberg, Avi Z. Jin, Shelly Roberts, David D.
Abstract	Thromobospondin-1 inhibits angiogenesis in part by interacting with the ubiquitous cell surface receptor CD47. In endothelial cells, CD47 interacts directly with vascular endothelial growth factor receptor-2 (VEGFR2), and thrombospondin-1 inhibits VEGFR2 phosphorylation and signaling by disrupting this association. We now show that CD47 similarly associates with and regulates VEGFR2 in T cells. Thrombospondin-1 inhibits phosphorylation of VEGFR2 and its downstream target Src in wild type but not in CD47-deficient human Jurkat and primary murine T cells. VEGFR2 signaling inhibits proliferation and TCR signaling in wild type T cells. However, ligation of CD47 by thrombospondin-1 or loss of CD47 expression reverses some inhibitory effects of VEGF on proliferation and T cell activation. We further found that VEGF and VEGFR2 expression are up-regulated in CD47-deficient murine CD4+ and human Jurkat T cells, and the resulting autocrine VEGFR2 signaling enhances proliferation and some TCR responses in the absence of CD47. Thus, CD47 signaling modulates the ability of VEGF to regulate proliferation and TCR signaling, and autocrine production of VEGF by T cells contributes to this regulation. This provides a mechanism to understand the context-dependent effects of thrombospondin-1 and VEGF on T cell activation and reveals an important role for CD47 signaling in regulating T cell production of the major angiogenic factor VEGF.
Related Links	http://dx.doi.org/10.4049/jimmunol.1303116
Ending Page	3924
Page Count	11
Starting Page	3914
File Format	PDF
ISSN	15506606
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	8
Volume Number	193
Language	English
Publisher Date	2014-10-15
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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