Thomas Jamieson1, 9, Donald N Cook2, 9, Robert J B Nibbs1, 3, Antal Rot4, Colin Nixon5, Pauline Mclean3, Antonio Alcami6, Sergio A Lira7, Maria Wiekowski8
& Gerard J Graham1, 31
The Beatson Institute for Cancer Research, Glasgow G61 1BD, UK.
2
Department of Medicine, Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27706, USA.
3
Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow G11 6NT, UK.
4
Novartis Institutes for Biomedical Research, Vienna A1230, Austria.
5
Department of Veterinary Pathology, University of Glasgow, Glasgow G61 1QH, UK.
6
Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología, Universidad Autónoma, Cantoblanco 28049 Madrid, Spain.
7
Immunobiology Center, Mount Sinai School of Medicine, New York, New York 10029, USA.
8
Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA.
9
These authors contributed equally to this work.
Correspondence should be addressed to Gerard J Graham g.graham@beatson.gla.ac.uk
-chemokines from cutaneous sites. After induction of inflammation by phorbol esters, wild-type mice showed a transient inflammatory response. However, in D6-deficient mice, an excess concentration of residual chemokines caused a notable inflammatory pathology with similarities to human psoriasis. These results suggest that D6 is involved in the resolution of the cutaneous inflammatory response.
