期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 8, 页码 5186-5194出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.8.5186
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- NCRR NIH HHS [P20RR15557] Funding Source: Medline
- NIAID NIH HHS [R01 AI 51468] Funding Source: Medline
Cystic fibrosis (CF) lung disease is characterized by persistent airway inflammation and airway infection that ultimately leads to respiratory failure. Aspergillus sp. are present in the airways of 20-40% of CF patients and are of unclear clinical significance. In this study, we demonstrate that CF transmembrane conductance regulator (CFTR)-deficient (CFTR knockout, Cftr(tm1Unc-) TgN(fatty acid-binding protein)CFTR) and mutant (Delta F508) mice develop profound lung inflammation in response to Aspergillus fumigatus hyphal Ag exposure. CFTR-deficient mice also develop an enhanced Th2 inflammatory response to A. fumigatus, characterized by elevated IL-4 in the lung and IgE and IgG1 in serum. In contrast, CFTR deficiency does not promote a Th1 immune response. Furthermore, we demonstrate that CD4(+) T cells from naive CFTR-deficient mice produce higher levels of IL-4 in response to TCR ligation than wild-type CD4(+) T cells. The Th2 bias of CD4(+) T cells in the absence of functional CFTR correlates with elevated nuclear levels of NFAT. Thus, CFTR is important to maintain the Th1/Th2 balance in CD4(+) T cells.
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