| First Author | Wortham BW | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 8 | Pages | 3227-31 |
| PubMed ID | 26927798 | Mgi Jnum | J:286240 |
| Mgi Id | MGI:6402677 | Doi | 10.4049/jimmunol.1500978 |
| Citation | Wortham BW, et al. (2016) CLEC5A Mediates Macrophage Function and Chronic Obstructive Pulmonary Disease Pathologies. J Immunol 196(8):3227-31 |
| abstractText | Chronic obstructive pulmonary disease (COPD) is a devastating disease with no effective therapies. We investigated the role of the C-type lectin receptor, CLEC5A, in macrophage activation and pulmonary pathogenesis in a mouse model of COPD. We demonstrate that CLEC5A is expressed on alveolar macrophages in mice exposed long-term to cigarette smoke (CS), as well as in human smokers. We also show that CLEC5A-mediated activation of macrophages enhanced cytokine elaboration alone, as well as in combination with LPS or GM-CSF in CS-exposed mice. Furthermore, usingClec5a-deficient mice, we demonstrate that CS-induced macrophage responsiveness is mediated by CLEC5A, and CLEC5A is required for the development of inflammation, proinflammatory cytokine expression, and airspace enlargement. These findings suggest a novel mechanism that promotes airway inflammation and pathologies in response to CS exposure and identifies CLEC5A as a novel target for the therapeutic control of COPD pathogenesis. |
