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Activators Inhibit IFN--Induced Expression of the T Cell-Active CXC Chemokines IP-10, Mig, and I-TAC in Human Endothelial Cells1
*
Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115;
Infectious Disease Unit, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129; and
Department of Neurosciences, The Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195
Peroxisome proliferator-activated receptor-
(PPAR), a member
of the nuclear hormone receptor superfamily originally shown to play an
important role in adipocyte differentiation and glucose homeostasis, is
now known to regulate inflammatory responses. Given the importance of
endothelial cell (EC)-derived chemokines in regulating leukocyte
function and trafficking, we studied the effects of PPAR ligands on
the expression of chemokines induced in ECs by the Th1 cytokine
IFN-. Treatment of ECs with PPAR activators significantly
inhibited IFN--induced mRNA and protein expression of the CXC
chemokines IFN-inducible protein of 10 kDa (IP-10), monokine induced by
IFN- (Mig), and IFN-inducible T-cell 
-chemoattractant (I-TAC),
whereas expression of the CC chemokine monocyte chemoattractant
protein-1 was not altered. PPAR activators decreased IFN-inducible
protein of 10 kDa promoter activity and inhibited protein binding to
the two NF-
B sites but not to the IFN-stimulated response element
ISRE site. Furthermore, PPAR ligands inhibited the release of
chemotactic activity for CXC chemokine receptor 3 (CXCR3)-transfected
lymphocytes from IFN--stimulated ECs. These data suggest that
anti-diabetic PPAR activators might attenuate the recruitment of
activated T cells at sites of Th1-mediated
inflammation.
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B. R. Kwak, S. Myit, F. Mulhaupt, N. Veillard, N. Rufer, E. Roosnek, and F. Mach PPAR{gamma} but not PPAR{alpha} Ligands Are Potent Repressors of Major Histocompatibility Complex Class II Induction in Atheroma-Associated Cells Circ. Res., February 22, 2002; 90(3): 356 - 362. [Abstract] [Full Text] [PDF]
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