| First Author | Chen LC | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 6 | Pages | 3025-8 |
| PubMed ID | 11544284 | Mgi Jnum | J:71495 |
| Mgi Id | MGI:2150236 | Doi | 10.4049/jimmunol.167.6.3025 |
| Citation | Chen LC, et al. (2001) Cutting edge: altered pulmonary eosinophilic inflammation in mice deficient for Clara cell secretory 10-kDa protein. J Immunol 167(6):3025-8 |
| abstractText | Clara cell secretory protein (CC10) is a steroid-inducible protein, and its in vivo function is currently unclear. The role of CC10 in modulation of pulmonary allergic inflammation was examined in mice deficient for the CC10 gene. Wild-type and homozygous CC10-deficient mice were sensitized with an Ag, OVA, and challenged with either OVA or saline. When compared with that seen in wild-type mice, a significantly higher level of pulmonary eosinophilia was found in Ag-sensitized and challenged CC10-deficient mice. Significantly increased levels of Th2 cytokines IL-4, IL-5, IL-9, and IL-13 were also found in CC10-deficient mice. In addition, an increased level of eotaxin, but not RANTES, was also seen in CC10-deficient mice. No significant difference was observed in the level of a Th1 cytokine, IFN-gamma, between different groups of mice. These results provided the first in vivo evidence that CC10 plays a role in the modulation of pulmonary allergic inflammation. |
