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Blood, 15 November 2004, Vol. 104, No. 10, pp. 3205-3213.
Prepublished online as a Blood First Edition Paper on July 27, 2004; DOI 10.1182/blood-2004-03-1184.
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Submitted March 30, 2004
Accepted June 29, 2004
Mouse CD99 participates in T cell recruitment into inflamed skin
Gabriele Bixel, Stephan Kloep, Stefan Butz, Bjorn Petri, Britta Engelhardt, and Dietmar Vestweber*
Max-Planck-Institute of Molecular Biomedicine, Munster, Germany
Institute of Cell Biology, University of Munster, Munster, Germany
Max-Planck-Institute of Molecular Biomedicine, Munster, Germany; Institute of Cell Biology, University of Munster, Munster, Germany
* Corresponding author; email: vestweb{at}uni-muenster.de.
Human CD99 is a small highly O-glycosylated cell surface protein expressed on most leukocytes. It was recently found to be expressed at endothelial cell contacts and to participate in the transendothelial migration (TEM) of monocytes in vitro. In order to analyse the physiological relevance of CD99 in vivo we searched for the mouse homolog. We cloned a mouse cDNA coding for a protein 45% identical in its sequence with human CD99. Based on the cDNA we generated antibodies against this mouse homolog of CD99, which detected the antigen on most leukocytes, on endothelia of various tissues and at cell contacts of cultured endothelial cells. Cell aggregation of CD99-transfected CHO cells was completely blocked by anti-CD99 antibodies. The same antibodies inhibited TEM of lymphocytes in vitro, independent of whether T cells or endothelial cells were preincubated with antibodies. In a cutaneous delayed-type hypersensitivity reaction (DTH), anti-CD99 antibodies inhibited the recruitment of in vivo activated T cells into inflamed skin as well as edema formation. We conclude that mouse CD99 participates in the TEM of lymphocytes and in their recruitment to inflamed skin in vivo. This establishes CD99 as a valid target for interference with cutaneous inflammatory processes.
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