T van Es

Publications (5)12.65 Total impact

• Article: Attenuated atherosclerosis upon IL-17R signaling disruption in LDLr deficient mice.

  T van Es, G H M van Puijvelde, O H Ramos, F M E Segers, L A Joosten, W B van den Berg, I M Michon, P de Vos, Th J C van Berkel, J Kuiper
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  ABSTRACT: Atherosclerosis is an inflammatory disease characterized by the influx of macrophages and T cells and IL-17 may connect innate and adaptive immune responses involved in atherogenesis. We investigated the role of IL-17 receptor signaling in atherosclerosis and transplanted LDLr deficient recipient mice with IL-17R deficient bone marrow. Induction of atherosclerosis by Western-type diet induced a 46% reduction in lesion size in the aortic root and the plaque composition revealed no significant changes in collagen content and neutrophil counts, but a reduction in mast cell number and an increase in macrophage number. In addition, we observed a decrease in anti-oxLDL antibodies of the IgG class upon IL-17R BMT, while introduction of IL-17R deficient bone marrow resulted in a reduced IL-6 production and an increased IL-10 production. In conclusion, signaling via the IL-17 receptor in bone marrow derived cells enhances the process of atherosclerosis.
  Biochemical and Biophysical Research Communications 09/2009; 388(2):261-5. · 2.48 Impact Factor
• Article: Vaccination against Foxp3(+) regulatory T cells aggravates atherosclerosis.

  T van Es, G H M van Puijvelde, A C Foks, K L L Habets, I Bot, E Gilboa, T J C Van Berkel, J Kuiper
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  ABSTRACT: Regulatory T cells are crucial for immune homeostasis and an impaired regulatory T cell function results in many pathological conditions. Regulatory T cells have already been described to be protective in atherosclerosis. However the exact contribution of Foxp3-expressing natural regulatory T cells in atherosclerosis has not been elucidated yet. In this study we vaccinated LDL receptor deficient mice with dendritic cells which are transfected with Foxp3 encoding mRNA and studied the effect on initial atherosclerosis. Vaccination against Foxp3 resulted in a reduction of Foxp3(+) regulatory T cells in several organs and in an increase in initial atherosclerotic lesion formation. Furthermore we observed an increase in plaque cellularity and increased T cell proliferation in the Foxp3 vaccinated mice. We further establish the protective role of Tregs in atherosclerosis. The results illustrate the important role for Foxp3-expressing regulatory T cells in atherosclerosis, thereby providing a potential opportunity for therapeutic intervention against this disease.
  Atherosclerosis 08/2009; 209(1):74-80. · 3.79 Impact Factor
• Source

  Available from: ahajournals.org

  Article: Induction of oral tolerance to HSP60 or an HSP60-peptide activates T cell regulation and reduces atherosclerosis.

  G H M van Puijvelde, T van Es, E J A van Wanrooij, K L L Habets, P de Vos, R van der Zee, W van Eden, Th J C van Berkel, J Kuiper
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  ABSTRACT: HSP60-specific T cells contribute to the development of the immune responses in atherosclerosis. This can be dampened by regulatory T cells activated via oral tolerance induction, and we explored the effect of oral tolerance induction to HSP60 and the peptide HSP60 (253 to 268) on atherosclerosis. HSP60 and HSP60 (253 to 268) were administered orally to LDLr(-/-) mice before induction of atherosclerosis and resulted in a significant 80% reduction in plaque size in the carotid arteries and in a 27% reduction in plaque size at the aortic root. Reduction in plaque size correlated with an increase in CD4(+)CD25(+)Foxp3(+) regulatory T cells in several organs and in an increased expression of Foxp3, CD25, and CTLA-4 in atherosclerotic lesions of HSP60-treated mice. The production of interleukin (IL)-10 and transforming growth factor (TGF)-beta by lymph node cells in response to HSP60 was observed after tolerance induction. Oral tolerance induction to HSP60 and a small HSP60-peptide leads to an increase in the number of CD4(+)CD25(+)Foxp3(+) regulatory T cells, resulting in a decrease in plaque size as a consequence of increased production of IL-10 and TGF-beta. We conclude that these beneficial results of oral tolerance induction to HSP60 and HSP60 (253 to 268) may provide new therapeutic approaches for the treatment of atherosclerosis.
  Arteriosclerosis Thrombosis and Vascular Biology 01/2008; 27(12):2677-83. · 6.37 Impact Factor
• Article: Induction of oral tolerance to HSP60 or an HSP60-peptide activates T cell regulation and reduces atherosclerosis

  G.H. van Puijvelde, T van Es, E.J. van Wanrooij, K.L. Habets, P. Vos, R van der Zee, W. van Eden, T J van Berkel, J Kuiper
• Article: Attenuated atherosclerosis upon IL-17R signaling disruption in LDLr deficient mice

  T. van Es, G.H.M. van Puijvelde, O.H. Ramos, F.M.E. Segers, L.A. Joosten, W.B. van den Berg, I.M. Michon, P. de Vos, Th.J.C. van Berkel, J. Kuiper
  [show abstract] [hide abstract]
  ABSTRACT: Atherosclerosis is an inflammatory disease characterized by the influx of macrophages and T cells and IL-17 may connect innate and adaptive immune responses involved in atherogenesis. We investigated the role of IL-17 receptor signaling in atherosclerosis and transplanted LDLr deficient recipient mice with IL-17R deficient bone marrow. Induction of atherosclerosis by Western-type diet induced a 46% reduction in lesion size in the aortic root and the plaque composition revealed no significant changes in collagen content and neutrophil counts, but a reduction in mast cell number and an increase in macrophage number. In addition, we observed a decrease in anti-oxLDL antibodies of the IgG class upon IL-17R BMT, while introduction of IL-17R deficient bone marrow resulted in a reduced IL-6 production and an increased IL-10 production.In conclusion, signaling via the IL-17 receptor in bone marrow derived cells enhances the process of atherosclerosis.
  Biochemical and Biophysical Research Communications.