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Platelet Endothelial Cell Adhesion Molecule Deficiency or Blockade Significantly Reduces Leukocyte Emigration in a Majority of Mouse Strains
Author(s) -
Alan R. Schenkel,
Tina W. Chew,
William A. Müller
Publication year - 2004
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.173.10.6403
Subject(s) - inflammation , knockout mouse , in vivo , strain (injury) , biology , immunology , platelet , in vitro , microbiology and biotechnology , function (biology) , receptor , biochemistry , genetics , anatomy
PECAM is a molecule used specifically during the diapedesis step when neutrophils and monocytes leave the blood compartment. Anti-PECAM reagents, such as Abs and soluble fusion proteins, block diapedesis both in vivo and in vitro. However, the PECAM knockout mouse in C57BL/6 strain has no serious defects in most models of inflammation. We show in this study that the same PECAM knockout backcrossed into the FVB/n strain clearly has reduced leukocyte emigration in two models of inflammation. Furthermore, we show that anti-PECAM reagents can block leukocyte emigration in several other wild-type strains of mice like FVB/n, SJL, and the outbred strain Swiss Webster. This clearly shows that the C57BL/6 strain is uniquely able to compensate for the loss of PECAM function. Murine models of inflammatory disease that have been studied using C57BL/6 mice should be re-evaluated using FVB/n or other mouse strains to determine whether PECAM plays a role in those models.

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