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Cutting Edge |
* Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology and
Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114
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
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.
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