Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 5, Pages 3524-3534Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.5.3524
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Funding
- Spanish Ministry of Education and Science [SAF2005-00241, NAN2004-08805-C04/04, SAF2006-07609]
- Fundacion para la Investigacion y Prevencion del SIDA en Espana [36550/06]
- La Marato TV3 Foundation
- Comunidad de Madrid [DIFHE-MAT-CM S-SAL-0304-2006]
- European Union [FP6 LSHB-CT-2005-518167]
- Spanish National Research Council
- Pfizer
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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.
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