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JCI online early table of contents: June 13, 2011
Date:6/13/2011

ombus-promoting TF is generated in vivo, is, however, not well defined. Now, Ruf and colleagues have identified a role for the protein P2X7 receptor in generating thrombus-promoting TF. Specifically, they found that signaling triggered by P2X7 receptor binding to the molecule ATP induced mouse myeloid cells to produce TF-positive microparticles. They therefore suggest that targeting P2X7 receptor may represent a new approach to anti-coagulant therapy.

TITLE: P2X7 receptor signaling contributes to tissue factordependent thrombosis in mice

AUTHOR CONTACT:
Wolfram Ruf
Scripps Research Institute, La Jolla, California, USA.
Phone: 858.784.2748; Fax: 858.784.8480; E-mail: ruf@scripps.edu.

View this article at: http://www.jci.org/articles/view/46129?key=85ec937aa7705ef4be8e


HEMATOLOGY: Stopping transplanted cells from attacking

One potential cure for several blood cell conditions (including some forms of leukemia) is transplantation with blood or bone marrow from a genetically non-identical individual (a treatment known as allogeneic BMT). One of the most severe complications of allogeneic BMT is graft-versus-host-disease (GVHD), which occurs if immune cells known as T cells in the transplanted blood or bone marrow attack the transplant recipient's body. A team of researchers, led by Markus Mapara, at the University of Pittsburgh, Pittsburgh, has now provided new insight into immune cell interactions that control the development of GVHD. Specifically, Mapara and colleagues found that lack of the protein STAT1 in CD4+ T cells in donor blood reduced the incidence of GVHD in mouse models of allogeneic BMT. While further analysis defined the cellular mechanisms underlying this effect, the authors suggest that targeting STAT1 in CD4+ T cells could provide therapeutic benefit.

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Journal of Clinical Investigation
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