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Altered Leukocyte Dynamics by PECAM‐deficient mice during Chemical Contact Hypersensitivity
Author(s) -
Schenkel Alan Rowe,
Unnithan Ranjana,
Early Merideth A,
Gilchrist John M.,
Schroeder William G.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.666.11
Subject(s) - cd8 , immunology , biology , flow cytometry , inflammation , cd3 , monocyte , cell adhesion molecule , cd31 , microbiology and biotechnology , immune system , immunohistochemistry
We have shown that Platelet Endothelial Cell Adhesion Molecule (PECAM, CD31) deficient mice in the FVB/n background have altered neutrophil and monocyte trafficking. These studies did not look at other leukocyte populations and relied typically on a primary inflammatory response. In this study, we used 2,4 Dinitrofluorobenzene (DNFB) to first sensitize wild type and PECAM deficient mice. Five days later, DNFB was applied to ears, and leukocytes from the ears were collected two days later. Major leukocyte populations were analyzed using six‐color flow‐cytometry. Some leukocyte populations, like dendritic cells and CD8+ T cells were unaffected by PECAM deficiency. Other populations, CD4+ T cells, gamma‐delta T cells, and DX5+, CD3− Natural Killer cells were markedly reduced in PECAM deficient mice. Another marker of inflammation, ear thickness, was unaffected by PECAM deficiency. These studies show that PECAM is differentially by some various leukocyte populations and may explain why some have little or no detectable PECAM expression in humans. This may have significant effects if anti‐PECAM therapies are used to selectively target certain leukocyte subsets.