|
|
Blood, 15 June 2007, Vol. 109, No. 12, pp. 5327-5336.
Prepublished online as a Blood First Edition Paper on March 7, 2007; DOI 10.1182/blood-2006-08-043109.
 Previous Article | Table of Contents | Next Article 
IMMUNOBIOLOGY
A CD99-related antigen on endothelial cells mediates neutrophil but not lymphocyte extravasation in vivo
M. Gabriele Bixel1,2,
Björn Petri2,
Alexander G. Khandoga3,
Andrej Khandoga3,
Karen Wolburg-Buchholz4,
Hartwig Wolburg4,
Sigrid März2,
Fritz Krombach3, and
Dietmar Vestweber1,2
1 Institute of Cell Biology, Zentrum für Molekularbiologie der Entzündung (ZMBE), Interdisziplinäres Klinisches Forschungszentrum Münster, University of Münster, Münster;
2 Max-Planck-Institute of Molecular Biomedicine, Münster;
3 Institute for Surgical Research, University of Munich, Munich; and
4 Institute of Pathology, University of Tübingen, Germany
CD99 is a long-known leukocyte antigen that does not belong to any of the known protein families. It was recently found on endothelial cells, where it mediates transendothelial migration of human monocytes and lymphocyte recruitment into inflamed skin in the mouse. Here, we show that CD99L2, a recently cloned, widely expressed antigen of unknown function with moderate sequence homology to CD99, is expressed on mouse leukocytes and endothelial cells. Using antibodies, we found that CD99L2 and CD99 are involved in transendothelial migration of neutrophils in vitro and in the recruitment of neutrophils into inflamed peritoneum. Intravital and electron microscopy of cremaster venules revealed that blocking CD99L2 inhibited leukocyte transmigration through the vessel wall (diapedesis) at the level of the perivascular basement membrane. We were surprised to find that, in contrast to CD99, CD99L2 was not relevant for the extravasation of lymphocytes into inflamed tissue. Although each protein promoted cell aggregation of transfected cells, endothelial CD99 and CD99L2 participated in neutrophil extravasation independent of these proteins on neutrophils. Our results establish CD99L2 as a new endothelial surface protein involved in neutrophil extravasation. In addition, this is the first evidence for a role of CD99 and CD99L2 in the process of leukocyte diapedesis in vivo.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
Related Article in Blood Online:
-
To transmigrate or not to transmigrate
- Klaus Ley
Blood 2007 109: 5072-5073.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
S. Yakubenia, D. Frommhold, D. Scholch, C. C. Hellbusch, C. Korner, B. Petri, C. Jones, U. Ipe, M. G. Bixel, R. Krempien, et al.
Leukocyte trafficking in a mouse model for leukocyte adhesion deficiency II/congenital disorder of glycosylation IIc
Blood,
August 15, 2008;
112(4):
1472 - 1481.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. J.A. van Wanrooij, P. de Vos, M. G. Bixel, D. Vestweber, T. J.C. van Berkel, and J. Kuiper
Vaccination against CD99 inhibits atherogenesis in low-density lipoprotein receptor-deficient mice
Cardiovasc Res,
June 1, 2008;
78(3):
590 - 596.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Z. Mamdouh, G. E. Kreitzer, and W. A. Muller
Leukocyte transmigration requires kinesin-mediated microtubule-dependent membrane trafficking from the lateral border recycling compartment
J. Exp. Med.,
April 14, 2008;
205(4):
951 - 966.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Woodfin, M.-B. Voisin, and S. Nourshargh
PECAM-1: A Multi-Functional Molecule in Inflammation and Vascular Biology
Arterioscler. Thromb. Vasc. Biol.,
December 1, 2007;
27(12):
2514 - 2523.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. M. Rao, L. Yang, G. Garcia-Cardena, and F. W. Luscinskas
Endothelial-Dependent Mechanisms of Leukocyte Recruitment to the Vascular Wall
Circ. Res.,
August 3, 2007;
101(3):
234 - 247.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
