Regulatory Role of CD4+ T Cells in Myocarditis
Myocarditis is an important cause of heart failure in young patients. Autoreactive, most often, infection-triggered CD4+ T cells were confirmed to be critical for myocarditis induction. Due to a defect in clonal deletion of heart-reactive CD4+ T cells in the thymus of mice and humans, significant nu...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2018/4396351 |
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| author | Daria Vdovenko Urs Eriksson |
| author_facet | Daria Vdovenko Urs Eriksson |
| author_sort | Daria Vdovenko |
| collection | DOAJ |
| description | Myocarditis is an important cause of heart failure in young patients. Autoreactive, most often, infection-triggered CD4+ T cells were confirmed to be critical for myocarditis induction. Due to a defect in clonal deletion of heart-reactive CD4+ T cells in the thymus of mice and humans, significant numbers of heart-specific autoreactive CD4+ T cells circulate in the blood. Normally, regulatory T cells maintain peripheral tolerance and prevent spontaneous myocarditis development. In the presence of tissue damage and innate immune activation, however, activated self-antigen-loaded dendritic cells promote CD4+ effector T cell expansion and myocarditis. So far, a direct pathogenic role has been described for both activated Th17 and Th1 effector CD4+ T cell subsets, though Th1 effector T cell-derived interferon-gamma was shown to limit myocarditis severity and prevent transition to inflammatory dilated cardiomyopathy. Interestingly, recent observations point out that various CD4+ T cell subsets demonstrate high plasticity in maintaining immune homeostasis and modulating disease phenotypes in myocarditis. These subsets include Th1 and Th17 effector cells and regulatory T cells, despite the fact that there are still sparse and controversial data on the specific role of FOXP3-expressing Treg in myocarditis. Understanding the specific roles of these T cell populations at different stages of the disease progression might provide a key for the development of successful therapeutic strategies. |
| format | Article |
| id | doaj-art-28031ee397c740a382dc1668a56079b2 |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-28031ee397c740a382dc1668a56079b22025-02-03T05:58:12ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/43963514396351Regulatory Role of CD4+ T Cells in MyocarditisDaria Vdovenko0Urs Eriksson1Cardioimmunology, Center for Molecular Cardiology, University of Zurich, Zurich, SwitzerlandCardioimmunology, Center for Molecular Cardiology, University of Zurich, Zurich, SwitzerlandMyocarditis is an important cause of heart failure in young patients. Autoreactive, most often, infection-triggered CD4+ T cells were confirmed to be critical for myocarditis induction. Due to a defect in clonal deletion of heart-reactive CD4+ T cells in the thymus of mice and humans, significant numbers of heart-specific autoreactive CD4+ T cells circulate in the blood. Normally, regulatory T cells maintain peripheral tolerance and prevent spontaneous myocarditis development. In the presence of tissue damage and innate immune activation, however, activated self-antigen-loaded dendritic cells promote CD4+ effector T cell expansion and myocarditis. So far, a direct pathogenic role has been described for both activated Th17 and Th1 effector CD4+ T cell subsets, though Th1 effector T cell-derived interferon-gamma was shown to limit myocarditis severity and prevent transition to inflammatory dilated cardiomyopathy. Interestingly, recent observations point out that various CD4+ T cell subsets demonstrate high plasticity in maintaining immune homeostasis and modulating disease phenotypes in myocarditis. These subsets include Th1 and Th17 effector cells and regulatory T cells, despite the fact that there are still sparse and controversial data on the specific role of FOXP3-expressing Treg in myocarditis. Understanding the specific roles of these T cell populations at different stages of the disease progression might provide a key for the development of successful therapeutic strategies.http://dx.doi.org/10.1155/2018/4396351 |
| spellingShingle | Daria Vdovenko Urs Eriksson Regulatory Role of CD4+ T Cells in Myocarditis Journal of Immunology Research |
| title | Regulatory Role of CD4+ T Cells in Myocarditis |
| title_full | Regulatory Role of CD4+ T Cells in Myocarditis |
| title_fullStr | Regulatory Role of CD4+ T Cells in Myocarditis |
| title_full_unstemmed | Regulatory Role of CD4+ T Cells in Myocarditis |
| title_short | Regulatory Role of CD4+ T Cells in Myocarditis |
| title_sort | regulatory role of cd4 t cells in myocarditis |
| url | http://dx.doi.org/10.1155/2018/4396351 |
| work_keys_str_mv | AT dariavdovenko regulatoryroleofcd4tcellsinmyocarditis AT urseriksson regulatoryroleofcd4tcellsinmyocarditis |