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Biomedical Research Centre and Department of Pathology and Laboratory Medicine, University of British Columbia, British Columbia, Canada
Using noncompetitive methodologies comparing CD43+/+ and CD43–/– mice, it has been reported that CD43–/– leukocytes exhibit reduced recruitment efficiency to sites of inflammation. More recent analyses demonstrate that CD43 on activated T cells can function as an E-selectin ligand (E-SelL) in vitro, suggesting that CD43 might promote rolling interactions during recruitment of leukocytes and account for the reported recruitment deficits in CD43–/– T cells and neutrophils in vivo. Internally controlled competitive in vivo methods using fluorescent tracking dyes were applied to compare recruitment efficiency of CD43+/+ vs CD43–/– activated T cells to inflamed skin and of peripheral blood neutrophils to inflamed peritoneum. A simple CFSE perfusion method was developed to distinguish arterial/venous vasculature and confirm appropriate extravasation through venules in a Con A-induced cutaneous inflammation model. In vivo recruitment of peripheral blood neutrophils to inflamed peritoneum was core 2 GlcNAcT-I dependent, but recruitment efficiency was not influenced by absence of CD43. There were also no significant differences in core 2 GlcNAcT-I-dependent, selectin-dependent, cutaneous recruitment of activated T cells from CD43+/+ and congenic CD43–/– mice in either B6 or P-selectin–/– recipients despite biochemical confirmation that a CD43-specific E-SelL was present on activated T cells. We conclude that recruitment of neutrophils and activated T cells in these in vivo models is not influenced by CD43 expression and that if CD43 on activated T cells performs an E-SelL function in vivo, it contributes in a limited physiological context.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by a grant from the Canadian Institutes for Health Research (Grant MOP-64267).
2 Address correspondence and reprint requests to Dr. Douglas A. Carlow, Biomedical Research Centre, 2222 Health Sciences Mall, Vancouver, British Columbia, Canada V6T-1Z3; E-mail address: doug{at}brc.ubc.ca or Dr. Hermann J. Ziltener, Biomedical Research Centre, 2222 Health Sciences Mall, Vancouver, British Columbia, Canada V6T-1Z3; E-mail address: Hermann{at}brc.ubc.ca
3 Abbreviations used in this paper: PSGL-1, P-selectin glycoprotein ligand 1; C2, core 2 GlcNAcT-I; CTO, cell tracker orange; E-SelL, E-selectin ligand; hIg, human Ig; IVM, intravital microscopy; LCMV, lymphocytic choriomeningitis virus; PBN, peripheral blood neutrophil; RB, rolling buffer.
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