| First Author | Mira E | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 5 | Pages | 3524-34 |
| PubMed ID | 18714025 | Mgi Jnum | J:138942 |
| Mgi Id | MGI:3806892 | Doi | 10.4049/jimmunol.181.5.3524 |
| Citation | Mira E, et al. (2008) Statins induce regulatory T cell recruitment via a CCL1 dependent pathway. J Immunol 181(5):3524-34 |
| abstractText | The statins, a group of inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A reductase, are reported to influence a variety of immune system activities through 3-hydroxy-3-methylglutaryl coenzyme A reductase-dependent and -independent mechanisms. How statin treatment regulates immune system function in vivo nonetheless remains to be fully defined. We analyzed the immunomodulatory effects of lovastatin in a Candida albicans-induced delayed-type hypersensitivity reaction in mice. In this model, lovastatin administration reduced the acute inflammatory response elicited by C. albicans challenge. This anti-inflammatory activity of lovastatin was associated with a shift from a Th1 to a Th2 immune response, as well as an increase in the percentage of regulatory T cells at the inflammation site and in the regional draining lymph node. The lovastatin-induced increase in regulatory T cells in the inflamed skin was dependent on expression of CCL1, a chemokine that is locally up-regulated by statin administration. The anti-inflammatory effect of lovastatin was abrogated in CCL1-deficient mice. These results suggest that local regulation of chemokine expression may be an important process in statin-induced modulation of the immune system. |
