T cell trafficking in allergic asthma: the ins and outs.
T cells are critical mediators of the allergic airway inflammation seen in asthma. Pathogenic allergen-specific T cells are generated in regional lymph nodes and are then recruited into the airway by chemoattractants produced by the asthmatic lung. These recruited effector T cells and their products then mediate the cardinal features of asthma: airway eosinophilia, mucus hypersecretion, and airway hyperreactivity. There has been considerable progress in delineating the molecular mechanisms that control T cell trafficking into peripheral tissue, including the asthmatic lung. In this review, we summarize these advances and formulate them into a working model that proposes that T cell trafficking into and out of the allergic lung is controlled by several discrete regulatory pathways that involve the collaboration of innate and acquired immune cells.
Medoff
Benjamin D
BD
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Thomas
Seddon Y
SY
Luster
Andrew D
AD
D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D018925:Chemokines / Q000276:immunology; D002633:Chemotaxis / Q000276:immunology*; D006801:Humans; D008168:Lung / Q000166:cytology / Q000276:immunology; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology; D018448:Models, Immunological; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
D018925:Chemokines