Display Settings:

Format

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
    Atherosclerosis. 2006 Jun;186(2):302-9. Epub 2005 Sep 8.

    Effect of atorvastatin on TH1 and TH2 cytokine secreting cells during T cell activation and differentiation.

    Source

    MRC Toxicology Unit, Hodgkin Building, University of Leicester, PO Box 138, Lancaster Road, Leicester LE1 9HN, UK.

    Abstract

    Statins, which are 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are the most effective agents for the lowering of cholesterol in clinical practice. In addition to their lipid-lowering properties, statins also have immunomodulatory activities. Animal studies have shown that statins promote a T helper 2 (T(H)2) bias and suppress the secretion of T helper 1 (T(H)1) cytokines. We therefore examine whether atorvastatin modulates the T(H)1/T(H)2 responses in human T cells. Using primary T cells as well as differentiated T(H)1 and T(H)2 cells, the immunomodulatory effect of atorvastatin on cells secreting IFN-gamma (T(H)1 response) and IL-4 (T(H)2 response) was investigated. Atorvastatin had no effect on cells secreting IFN-gamma and IL-4 in primary T cells stimulated with anti-CD3 and -CD28 antibodies. Similarly, cells producing IFN-gamma and IL-4 in stable differentiated T(H)1 and T(H)2 cells were unaffected by atorvastatin. Furthermore, atorvastatin had no effect on the ratio of IFN-gamma+/IL-4+ cells during the differentiation of T(H)0 cells to T(H)1 and T(H)2 cells in long-term cultures. These data suggest that atorvastatin does not have any immunomodulatory effect on the T(H)1/T(H)2 balance in human T cells in vitro.

    Comment in

    PMID:
    16154133
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for Elsevier Science

      Save items

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk