The Journal of Experimental Medicine
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Published 19 November 2001. doi:10.1084/jem.194.10.1541
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© Rockefeller University Press, 0022-1007/2001/11/1541/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 10, November 19, 2001 1541-1547

Brief Definitive Report

CC Chemokine Receptor (CCR)4 and the CCR10 Ligand Cutaneous T Cell–attracting Chemokine (CTACK) in Lymphocyte Trafficking to Inflamed Skin

Yvonne Reiss1,2, Amanda E. Proudfoot4, Christine A. Power4, James J. Campbell3 and Eugene C. Butcher1,2

1 Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305
2 Veteran Affairs Palo Alto Health Care System, Palo Alto, CA 94304
3 Children's Hospital, Harvard Medical School, Boston, MA 02115
4 Serono Pharmaceutical Research Institute, Geneva 1205, Switzerland

Address correspondence to James J. Campbell, Assistant Professor of Pathology, Children's Hospital, 300 Longwood Ave., Bader Building No. 401, Boston, MA 02115. Phone: 617-355-8319; Fax: 617-738-6142; E-mail: james.campbell{at}tch.harvard.edu

The chemokine thymus and activation-regulated chemokine (TARC; CCL17) is displayed by cutaneous (but not intestinal) venules, and is thought to trigger vascular arrest of circulating skin homing memory T cells, which uniformly express the TARC receptor CC chemokine receptor (CCR)4. Cutaneous T cell–attracting chemokine (CTACK; CCL27), expressed by skin keratinocytes, also attracts cutaneous memory T cells, and is hypothesized to assist in lymphocyte recruitment to skin as well. Here we show that chronic cutaneous inflammation induces CD4 T cells expressing E-selectin binding activity (a marker of skin homing memory cells) in draining lymph node, and that these E-selectin ligand+ T cells migrate efficiently to TARC and to CTACK. In 24 h in vivo homing assays, stimulated lymph node T cells from wild-type mice or, surprisingly, from CCR4-deficient donors migrate efficiently to inflamed skin; and an inhibitory anti-CTACK antibody has no effect on wild-type lymphocyte recruitment. However, inhibition with anti-CTACK monoclonal antibody abrogates skin recruitment of CCR4-deficient T cells. We conclude that CTACK and CCR4 can both support homing of T cells to skin, and that either one or the other is required for lymphocyte recruitment in cutaneous delayed type hypersensitivity.

Key Words: lymphocyte homing • chemokines • inflammation • delayed type hypersensitivity • selectins


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