title: Cutting edge: Th2 cell trafficking into the allergic lung is dependent on chemoattractant receptor signaling.
abstract: Th2 cells are recruited to the lung where they mediate the asthma phenotype. Since the molecular mechanisms regulating Th2 cell trafficking remain unknown, we sought to determine whether trafficking of Th2 cells into the lung is mediated by G alpha i-coupled chemoattractant receptors. We show here that in contrast to untreated Th2 cells, pertussis toxin-treated Th2 cells were unable to traffic into the lung, airways, or lymph nodes following Ag challenge and therefore were unable to induce allergic inflammation in vivo. Pertussis toxin-treated Th2 cells were functional cells, however, and when directly instilled into the airways of mice, bypassing their need to traffic to the lung, were able to induce airway eosinophilic inflammation. These studies conclusively demonstrate that trafficking of Th2 cells into the lung is an active process dependent on chemoattractant receptors.
authors.affiliation: Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
authors.forename: Anuja
authors.initials: A
authors.lastname: Mathew
authors.forename: Benjamin D
authors.initials: BD
authors.lastname: Medoff
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Carafone
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Luster
mesh_terms: D019264:Adoptive Transfer; D000336:Aerosols; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D002464:Cell Migration Inhibition; D002465:Cell Movement / Q000276:immunology*; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D018984:Epitopes, T-Lymphocyte / Q000008:administration & dosage / Q000276:immunology; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D016023:Integrins / Q000096:biosynthesis; D007442:Intubation, Intratracheal; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008212:Lymphocyte Depletion; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D009093:Mucus / Q000378:metabolism; D009330:Nebulizers and Vaporizers; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D037342:Pertussis Toxin; D011657:Pulmonary Eosinophilia / Q000276:immunology / Q000473:pathology; D019707:Receptors, Chemokine / Q000502:physiology*; D012130:Respiratory Hypersensitivity / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology / Q000637:transplantation; D010566:Virulence Factors, Bordetella / Q000008:administration & dosage / Q000276:immunology / Q000494:pharmacology
chemical_list: D000336:Aerosols; D016207:Cytokines; D018984:Epitopes, T-Lymphocyte; D016023:Integrins; D019707:Receptors, Chemokine; D010566:Virulence Factors, Bordetella; D010047:Ovalbumin; D037342:Pertussis Toxin