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*
Institute for Lung Health and Division of Respiratory Medicine, Leicester University School of Medicine, Leicester, United Kingdom;
Harvard Medical School, Department of Pathology and Children’s Hospital, Division of Transfusion Medicine, Boston, MA 02115;
Laboratory of Immunology and Vascular Biology, Department of Pathology and the Digestive Disease Center, Department of Medicine, Stanford University Medical School, Stanford, CA 94305, and the Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Healthcare System, Palo Alto, CA 94304; and
§
Millenium Pharmaceuticals, Cambridge, MA 02142
The lung is an important tertiary lymphoid organ with constant
trafficking of T cells through the lung in both health and disease. T
cell migration is controlled by a combination of adhesion receptors and
chemokines expressed on vascular endothelium and in the tissue, often
in an organ-specific manner. This leads to selective accumulation of
different T cell subsets, a process called lymphocyte homing. There is
evidence for a distinct lung-homing pathway, but no specific
lung-homing receptors have been described. We analyzed the chemokine
receptor profile of lung T cells to determine the extent to which lung
T cells shared homing pathways with other organs such as the gut and
skin. In addition, we compared expression of receptors in normal and
asthmatic individuals to determine whether different pathways were used
in health and disease. We observed that lung T cells expressed a
profile of chemokine and adhesion receptors distinct from that of gut-
and skin-homing T cells although no chemokine receptor specific for the
lung was found. In particular, lung T cells expressed CCR5 and CXCR3,
but not CCR9 or cutaneous lymphocyte Ag, and only low levels of CCR4
and 
4
7. No differences were observed
between lung T cells from normal vs asthmatic subjects. This study
provides added support for the concept of a lung-homing pathway
separate from other mucosal organs such as the gut and suggests that
the chemokine pathways that control T cell migration in normal
homeostasis and Th2-type inflammatory responses are
similar.
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