Selective EGF-Receptor Inhibition in CD4 + T Cells Induces Anergy and Limits Atherosclerosis
Several epidermal growth factor receptor (EGFR) inhibitors have been successfully developed for the treatment of cancer, limiting tumor growth and metastasis. EGFR is also expressed by leukocytes, but little is known about its role in the modulation of the immune response. The aim of this study was...
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| Veröffentlicht in: | Journal of the American College of Cardiology Jg. 71; H. 2; S. 160 |
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16.01.2018
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| Abstract | Several epidermal growth factor receptor (EGFR) inhibitors have been successfully developed for the treatment of cancer, limiting tumor growth and metastasis. EGFR is also expressed by leukocytes, but little is known about its role in the modulation of the immune response.
The aim of this study was to determine whether EGFR expressed on CD4
T cells is functional and to address the consequences of EGFR inhibition in atherosclerosis, a T cell-mediated vascular chronic inflammatory disease.
The authors used EGFR tyrosine kinase inhibitors (AG-1478, erlotinib) and chimeric Ldlr
Cd4-Cre/Egfr
mouse with a specific deletion of EGFR in CD4
T cells.
Mouse CD4
T cells expressed EGFR, and the EGFR tyrosine kinase inhibitor AG-1478 blocked in vitro T cell proliferation and Th1/Th2 cytokine production. In vivo, treatment of Ldlr
mice with the EGFR inhibitor erlotinib induced T cell anergy, reduced T cell infiltration within atherosclerotic lesions, and protected against atherosclerosis development and progression. Selective deletion of EGFR in CD4
T cells resulted in decreased T cell proliferation and activation both in vitro and in vivo, as well as reduced interferon-γ, interleukin-4, and interleukin-2 production. Atherosclerotic lesion size was reduced by 2-fold in irradiated Ldlr
mice reconstituted with bone marrow from Cd4-Cre/Egfr
mice, compared to Cd4-Cre/Egfr
chimeric mice, after 4, 6, and 12 weeks of high-fat diet, associated with marked reduction in T cell infiltration in atherosclerotic plaques. Human blood T cells expressed EGFR and EGFR inhibition reduced T cell proliferation both in vitro and in vivo.
EGFR blockade induced T cell anergy in vitro and in vivo and reduced atherosclerosis development. Targeting EGFR may be a novel strategy to combat atherosclerosis. |
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| AbstractList | Several epidermal growth factor receptor (EGFR) inhibitors have been successfully developed for the treatment of cancer, limiting tumor growth and metastasis. EGFR is also expressed by leukocytes, but little is known about its role in the modulation of the immune response.BACKGROUNDSeveral epidermal growth factor receptor (EGFR) inhibitors have been successfully developed for the treatment of cancer, limiting tumor growth and metastasis. EGFR is also expressed by leukocytes, but little is known about its role in the modulation of the immune response.The aim of this study was to determine whether EGFR expressed on CD4+ T cells is functional and to address the consequences of EGFR inhibition in atherosclerosis, a T cell-mediated vascular chronic inflammatory disease.OBJECTIVESThe aim of this study was to determine whether EGFR expressed on CD4+ T cells is functional and to address the consequences of EGFR inhibition in atherosclerosis, a T cell-mediated vascular chronic inflammatory disease.The authors used EGFR tyrosine kinase inhibitors (AG-1478, erlotinib) and chimeric Ldlr-/-Cd4-Cre/Egfrlox/lox mouse with a specific deletion of EGFR in CD4+ T cells.METHODSThe authors used EGFR tyrosine kinase inhibitors (AG-1478, erlotinib) and chimeric Ldlr-/-Cd4-Cre/Egfrlox/lox mouse with a specific deletion of EGFR in CD4+ T cells.Mouse CD4+ T cells expressed EGFR, and the EGFR tyrosine kinase inhibitor AG-1478 blocked in vitro T cell proliferation and Th1/Th2 cytokine production. In vivo, treatment of Ldlr-/- mice with the EGFR inhibitor erlotinib induced T cell anergy, reduced T cell infiltration within atherosclerotic lesions, and protected against atherosclerosis development and progression. Selective deletion of EGFR in CD4+ T cells resulted in decreased T cell proliferation and activation both in vitro and in vivo, as well as reduced interferon-γ, interleukin-4, and interleukin-2 production. Atherosclerotic lesion size was reduced by 2-fold in irradiated Ldlr-/- mice reconstituted with bone marrow from Cd4-Cre/Egfrlox/lox mice, compared to Cd4-Cre/Egfr+/+ chimeric mice, after 4, 6, and 12 weeks of high-fat diet, associated with marked reduction in T cell infiltration in atherosclerotic plaques. Human blood T cells expressed EGFR and EGFR inhibition reduced T cell proliferation both in vitro and in vivo.RESULTSMouse CD4+ T cells expressed EGFR, and the EGFR tyrosine kinase inhibitor AG-1478 blocked in vitro T cell proliferation and Th1/Th2 cytokine production. In vivo, treatment of Ldlr-/- mice with the EGFR inhibitor erlotinib induced T cell anergy, reduced T cell infiltration within atherosclerotic lesions, and protected against atherosclerosis development and progression. Selective deletion of EGFR in CD4+ T cells resulted in decreased T cell proliferation and activation both in vitro and in vivo, as well as reduced interferon-γ, interleukin-4, and interleukin-2 production. Atherosclerotic lesion size was reduced by 2-fold in irradiated Ldlr-/- mice reconstituted with bone marrow from Cd4-Cre/Egfrlox/lox mice, compared to Cd4-Cre/Egfr+/+ chimeric mice, after 4, 6, and 12 weeks of high-fat diet, associated with marked reduction in T cell infiltration in atherosclerotic plaques. Human blood T cells expressed EGFR and EGFR inhibition reduced T cell proliferation both in vitro and in vivo.EGFR blockade induced T cell anergy in vitro and in vivo and reduced atherosclerosis development. Targeting EGFR may be a novel strategy to combat atherosclerosis.CONCLUSIONSEGFR blockade induced T cell anergy in vitro and in vivo and reduced atherosclerosis development. Targeting EGFR may be a novel strategy to combat atherosclerosis. Several epidermal growth factor receptor (EGFR) inhibitors have been successfully developed for the treatment of cancer, limiting tumor growth and metastasis. EGFR is also expressed by leukocytes, but little is known about its role in the modulation of the immune response. The aim of this study was to determine whether EGFR expressed on CD4 T cells is functional and to address the consequences of EGFR inhibition in atherosclerosis, a T cell-mediated vascular chronic inflammatory disease. The authors used EGFR tyrosine kinase inhibitors (AG-1478, erlotinib) and chimeric Ldlr Cd4-Cre/Egfr mouse with a specific deletion of EGFR in CD4 T cells. Mouse CD4 T cells expressed EGFR, and the EGFR tyrosine kinase inhibitor AG-1478 blocked in vitro T cell proliferation and Th1/Th2 cytokine production. In vivo, treatment of Ldlr mice with the EGFR inhibitor erlotinib induced T cell anergy, reduced T cell infiltration within atherosclerotic lesions, and protected against atherosclerosis development and progression. Selective deletion of EGFR in CD4 T cells resulted in decreased T cell proliferation and activation both in vitro and in vivo, as well as reduced interferon-γ, interleukin-4, and interleukin-2 production. Atherosclerotic lesion size was reduced by 2-fold in irradiated Ldlr mice reconstituted with bone marrow from Cd4-Cre/Egfr mice, compared to Cd4-Cre/Egfr chimeric mice, after 4, 6, and 12 weeks of high-fat diet, associated with marked reduction in T cell infiltration in atherosclerotic plaques. Human blood T cells expressed EGFR and EGFR inhibition reduced T cell proliferation both in vitro and in vivo. EGFR blockade induced T cell anergy in vitro and in vivo and reduced atherosclerosis development. Targeting EGFR may be a novel strategy to combat atherosclerosis. |
| Author | Friard, Jonas Guyonnet, Lea Joffre, Jeremie Guérin, Coralie Maître, Mikael Ait-Oufella, Hafid Nour-Eldine, Wared Tedgui, Alain Zeboudj, Lynda Mallat, Ziad Laurans, Ludivine Tharaux, Pierre-Louis Bourcier, Simon Lemarie, Jeremie Wakkach, Abdelilah Fabre, Elizabeth |
| Author_xml | – sequence: 1 givenname: Lynda surname: Zeboudj fullname: Zeboudj, Lynda organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 2 givenname: Mikael surname: Maître fullname: Maître, Mikael organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 3 givenname: Lea surname: Guyonnet fullname: Guyonnet, Lea organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 4 givenname: Ludivine surname: Laurans fullname: Laurans, Ludivine organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 5 givenname: Jeremie surname: Joffre fullname: Joffre, Jeremie organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 6 givenname: Jeremie surname: Lemarie fullname: Lemarie, Jeremie organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 7 givenname: Simon surname: Bourcier fullname: Bourcier, Simon organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 8 givenname: Wared surname: Nour-Eldine fullname: Nour-Eldine, Wared organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 9 givenname: Coralie surname: Guérin fullname: Guérin, Coralie organization: Luxembourg Institute of Health, Department of Infection and Immunity, Strassen, Luxembourg – sequence: 10 givenname: Jonas surname: Friard fullname: Friard, Jonas organization: CNRS, LP2M, UMR 7370, Faculté de Médecine, Université de Nice Sophia Antipolis, Nice, France – sequence: 11 givenname: Abdelilah surname: Wakkach fullname: Wakkach, Abdelilah organization: CNRS, LP2M, UMR 7370, Faculté de Médecine, Université de Nice Sophia Antipolis, Nice, France – sequence: 12 givenname: Elizabeth surname: Fabre fullname: Fabre, Elizabeth organization: Department of Medical Oncology, Hôpital Europeen G. Pompidou, AP-HP, Paris, France – sequence: 13 givenname: Alain surname: Tedgui fullname: Tedgui, Alain organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 14 givenname: Ziad surname: Mallat fullname: Mallat, Ziad organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France; Division of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, United Kingdom – sequence: 15 givenname: Pierre-Louis surname: Tharaux fullname: Tharaux, Pierre-Louis organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France – sequence: 16 givenname: Hafid surname: Ait-Oufella fullname: Ait-Oufella, Hafid email: hafid.aitoufella@inserm.fr organization: Inserm U970, Paris Cardiovascular Research Center, Paris, France; Université René Descartes, Paris, France; Service de Réanimation Médicale, Hôpital Saint-Antoine, AP-HP, Université Pierre-et-Marie Curie, Paris, France. Electronic address: hafid.aitoufella@inserm.fr |
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| Keywords | atherosclerosis immunity inflammation lymphocyte |
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| SubjectTerms | Animals Antineoplastic Agents - pharmacology Atherosclerosis - immunology CD4-Positive T-Lymphocytes - immunology Cytokines - analysis Cytokines - classification Cytokines - immunology ErbB Receptors - antagonists & inhibitors Erlotinib Hydrochloride - pharmacology Immunity, Cellular - drug effects Immunity, Cellular - immunology Mice Plaque, Atherosclerotic - drug therapy Plaque, Atherosclerotic - immunology Plaque, Atherosclerotic - pathology Protein Kinase Inhibitors - pharmacology T-Lymphocytes, Regulatory - immunology |
| Title | Selective EGF-Receptor Inhibition in CD4 + T Cells Induces Anergy and Limits Atherosclerosis |
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