| First Author | Kitamura H | Year | 2011 |
| Journal | J Clin Invest | Volume | 121 |
| Issue | 7 | Pages | 2863-75 |
| PubMed ID | 21646718 | Mgi Jnum | J:175658 |
| Mgi Id | MGI:5286813 | Doi | 10.1172/JCI45589 |
| Citation | Kitamura H, et al. (2011) Mouse and human lung fibroblasts regulate dendritic cell trafficking, airway inflammation, and fibrosis through integrin alphavbeta8-mediated activation of TGF-beta. J Clin Invest 121(7):2863-75 |
| abstractText | The airway is a primary portal of entry for noxious environmental stimuli that can trigger airway remodeling, which contributes significantly to airway obstruction in chronic obstructive pulmonary disease (COPD) and chronic asthma. Important pathologic components of airway remodeling include fibrosis and abnormal innate and adaptive immune responses. The positioning of fibroblasts in interstitial spaces suggests that they could participate in both fibrosis and chemokine regulation of the trafficking of immune cells such as dendritic cells, which are crucial antigen-presenting cells. However, physiological evidence for this dual role for fibroblasts is lacking. Here, in two physiologically relevant models - conditional deletion in mouse fibroblasts of the TGF-beta-activating integrin alphavbeta8 and neutralization of alphavbeta8 in human COPD fibroblasts |
