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T-cell derived interferon-gamma contributes to arteriolar dysfunction during acute hypercholesterolemia.

Karen Y Stokes1, Shelly Gurwara, D Neil Granger

  • 1Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, 1501 E Kings Highway, Shreveport, LA 71130-3932, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 23, 2007
PubMed
Summary

T-lymphocytes produce interferon-gamma (IFN-gamma), which drives endothelial dysfunction and blood cell adhesion in hypercholesterolemia. This study confirms T-cell IFN-gamma

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Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Vascular Inflammation

Background:

  • Hypercholesterolemia is linked to leukocyte recruitment in postcapillary venules.
  • T-lymphocytes and interferon-gamma (IFN-gamma) are implicated in this inflammatory process.

Purpose of the Study:

  • To determine if T-lymphocytes are the primary source of IFN-gamma during hypercholesterolemia.
  • To investigate whether T-cell-derived IFN-gamma mediates arteriolar dysfunction and platelet adhesion.

Main Methods:

  • Intravital videomicroscopy was employed to assess arteriolar responses to acetylcholine.
  • Leukocyte and platelet adhesion were quantified in postcapillary venules of wild-type, immunodeficient (SCID), and IFN-gamma knockout mice fed normal or high-cholesterol diets.
  • T-cell transfer experiments were conducted in immunodeficient mice.

Main Results:

  • Endothelial dysfunction, characterized by impaired acetylcholine-induced arteriolar dilation, was observed in hypercholesterolemic wild-type mice but absent in SCID or IFN-gamma knockout mice.
  • This dysfunction was transferable via wild-type T-cells, but not IFN-gamma-deficient T-cells.
  • Hypercholesterolemic wild-type mice showed increased leukocyte and platelet adhesion, which was reduced in SCID and IFN-gamma knockout mice and restored by wild-type T-cell transfer.

Conclusions:

  • T-lymphocyte-derived IFN-gamma plays a critical role in hypercholesterolemia-induced endothelial dysfunction in arterioles.
  • IFN-gamma mediates both inflammatory and thrombotic responses in postcapillary venules during hypercholesterolemia.