| First Author | Lukacs NW | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 4 | Pages | 551-5 |
| PubMed ID | 11514610 | Mgi Jnum | J:71096 |
| Mgi Id | MGI:2149176 | Doi | 10.1084/jem.194.4.551 |
| Citation | Lukacs NW, et al. (2001) Requirement for the chemokine receptor CCR6 in allergic pulmonary inflammation. J Exp Med 194(4):551-5 |
| abstractText | Allergic asthmatic responses in the airway are associated with airway hyperreactivity, eosinophil accumulation in the lung, and cytokine production by allergen-specific, T helper cell type 2 (Th2) lymphocytes. Here, we show that in a cockroach antigen (CA) model of allergic pulmonary inflammation, the chemokine macrophage inflammatory protein (MIP)-3alpha is expressed in the lung within hours of allergen challenge. To determine the biologic relevance of this expression, mice lacking CCR6, the only known receptor for MIP-3alpha, were studied for their response to CA. CCR6-deficient mice were immunized to the same extent as their wild-type counterparts, as judged by cytokine production in antigen-challenged lymphocytes. However, compared with CA-challenged wild-type mice, challenged CCR6-deficient mice had reduced airway resistance, fewer eosinophils around the airway, lower levels of interleukin 5 in the lung, and reduced serum levels of immunoglobulin E. Together, these data demonstrate that MIP-3alpha and CCR6 function in allergic pulmonary responses and suggest that these molecules might represent novel therapeutic targets for treatment of asthma. |
