Expression of chemokine receptors by lung T cells from normal and asthmatic subjects

Citation
Jj. Campbell et al., Expression of chemokine receptors by lung T cells from normal and asthmatic subjects, J IMMUNOL, 166(4), 2001, pp. 2842-2848
Citations number
30
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
166
Issue
4
Year of publication
2001
Pages
2842 - 2848
Database
ISI
SICI code
0022-1767(20010215)166:4<2842:EOCRBL>2.0.ZU;2-4
Abstract
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 mann er. This leads to selective accumulation of different T cell subsets, a pro cess called lymphocyte homing. There is evidence for a distinct lung-homing pathway, but no specific lung-homing receptors have been described. We ana lyzed the chemokine receptor profile of lung T cells to determine the exten t to which lung T cells shared homing pathways with other organs such as th e 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 o f chemokine and adhesion receptors distinct from that of gut- and skin-homi ng T cells although no chemokine receptor specific for the lung was found. In particular, lung T cells expressed CCR5 and CXCR3, but not CeR9 or cutan eous lymphocyte Ag, and only low levels of CCR4 and alpha (4)beta (7). No d ifferences were observed between lung T cells from normal vs asthmatic subj ects. This study provides added support far the concept of a lung-homing pa thway 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.