期刊
JOURNAL OF IMMUNOLOGY
卷 169, 期 2, 页码 651-655出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.2.651
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资金
- NHLBI NIH HHS [F32-HL10375] Funding Source: Medline
- NIAID NIH HHS [F32-AI50399, R01-AI40618] Funding Source: Medline
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 Galphai-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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