| First Author | Kallal LE | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 4 | Pages | 1042-52 |
| PubMed ID | 20101616 | Mgi Jnum | J:159194 |
| Mgi Id | MGI:4441567 | Doi | 10.1002/eji.200939778 |
| Citation | Kallal LE, et al. (2010) CCL20/CCR6 blockade enhances immunity to RSV by impairing recruitment of DC. Eur J Immunol 40(4):1042-52 |
| abstractText | Chemokines are important mediators of the immune response to pathogens, but can also promote chronic inflammatory states. Chemokine receptor 6 (CCR6) is found on immature DC and effector/memory T cells, and binds a single ligand, CCL20, with high affinity. Here, we investigated the role of CCL20 and CCR6 in a pulmonary viral infection caused by RSV, a ubiquitous virus that can cause severe pulmonary complications. Neutralization of CCL20 during RSV infection significantly reduced lung pathology and favored a Th1 effector response. CCR6-deficient animals recapitulated this phenotype, and additionally showed enhanced viral clearance when compared with WT mice. No differences were observed in migration of T cells to the lungs of CCR6(-/-) animals; however, a significant reduction was observed in numbers of conventional DC (cDC), but not plasmacytoid DC, in CCR6(-/-) mice. A pathogenic phenotype could be reconstituted in CCR6(-/-) mice by supplying cDC into the airway, indicating that mere number of cDC dictates the adverse response. Our data suggest that blockade of the CCL20/CCR6 pathway provides an environment whereby the attenuated recruitment of cDC alters the balance of innate immune cells and mediates the efficient antiviral response to RSV. |
