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Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice
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| Zeitschriftentitel: | Journal of Virology |
|---|---|
| Personen und Körperschaften: | , |
| In: | Journal of Virology, 64, 1990, 12, S. 5708-5715 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society for Microbiology
|
| Schlagwörter: |
| author_facet |
Baek, H S Yoon, J W Baek, H S Yoon, J W |
|---|---|
| author |
Baek, H S Yoon, J W |
| spellingShingle |
Baek, H S Yoon, J W Journal of Virology Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice Virology Insect Science Immunology Microbiology |
| author_sort |
baek, h s |
| spelling |
Baek, H S Yoon, J W 0022-538X 1098-5514 American Society for Microbiology Virology Insect Science Immunology Microbiology http://dx.doi.org/10.1128/jvi.64.12.5708-5715.1990 <jats:p>Pancreatic islets from SJL/J mice infected with the D variant of encephalomyocarditis virus (EMC-D virus) showed lymphocytic infiltration with moderate to severe destruction of beta cells. Immunohistochemical staining of the islet sections with several monoclonal antibodies, anti-Mac-1, anti-Mac-2, and F4/80 for macrophages, anti-L3T4 for helper/inducer T cells, and anti-Lyt2 for cytotoxic/suppressor T cells revealed that the major population of infiltrating cells at the early stage of viral infection was Mac-2-positive macrophages. In contrast, macrophages detected by anti-Mac-1 and F4/80 monoclonal antibodies were not found at the early stage of viral infection but were found at intermediate and late stages of viral infection. Helper/inducer T cells and cytotoxic/suppressor T cells also infiltrated the islets at intermediate and late stages of viral infection. Short-term treatment of mice with silica prior to viral infection resulted in an enhancement of beta-cell destruction, leading to the development of diabetes. In contrast, long-term treatment of mice with silica resulted in complete prevention of diabetes caused by a low dose of viral infection and a significant decrease in the incidence of diabetes caused by an intermediate or high dose of viral infection. Furthermore, depletion of macrophages by a specific monoclonal antibody (anti-Mac-2) resulted in a much greater decrease in the incidence of diabetes caused by an intermediate dose of viral infection. However, suppression of helper/inducer T cells and cytotoxic/suppressor T cells, by anti-L3T4 and anti-Lyt2 antibodies, respectively, did not alter the incidence of diabetes. On the basis of these data, it is concluded that macrophages, particularly Mac-2-positive macrophages, play a crucial role in the process of pancreatic beta-cell destruction at the early stage of encephalomyocarditis D virus infection in SJL/J mice.</jats:p> Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice Journal of Virology |
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| title |
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_unstemmed |
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_full |
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_fullStr |
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_full_unstemmed |
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_short |
Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_sort |
role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| topic |
Virology Insect Science Immunology Microbiology |
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http://dx.doi.org/10.1128/jvi.64.12.5708-5715.1990 |
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1990 |
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5708-5715 |
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<jats:p>Pancreatic islets from SJL/J mice infected with the D variant of encephalomyocarditis virus (EMC-D virus) showed lymphocytic infiltration with moderate to severe destruction of beta cells. Immunohistochemical staining of the islet sections with several monoclonal antibodies, anti-Mac-1, anti-Mac-2, and F4/80 for macrophages, anti-L3T4 for helper/inducer T cells, and anti-Lyt2 for cytotoxic/suppressor T cells revealed that the major population of infiltrating cells at the early stage of viral infection was Mac-2-positive macrophages. In contrast, macrophages detected by anti-Mac-1 and F4/80 monoclonal antibodies were not found at the early stage of viral infection but were found at intermediate and late stages of viral infection. Helper/inducer T cells and cytotoxic/suppressor T cells also infiltrated the islets at intermediate and late stages of viral infection. Short-term treatment of mice with silica prior to viral infection resulted in an enhancement of beta-cell destruction, leading to the development of diabetes. In contrast, long-term treatment of mice with silica resulted in complete prevention of diabetes caused by a low dose of viral infection and a significant decrease in the incidence of diabetes caused by an intermediate or high dose of viral infection. Furthermore, depletion of macrophages by a specific monoclonal antibody (anti-Mac-2) resulted in a much greater decrease in the incidence of diabetes caused by an intermediate dose of viral infection. However, suppression of helper/inducer T cells and cytotoxic/suppressor T cells, by anti-L3T4 and anti-Lyt2 antibodies, respectively, did not alter the incidence of diabetes. On the basis of these data, it is concluded that macrophages, particularly Mac-2-positive macrophages, play a crucial role in the process of pancreatic beta-cell destruction at the early stage of encephalomyocarditis D virus infection in SJL/J mice.</jats:p> |
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| description | <jats:p>Pancreatic islets from SJL/J mice infected with the D variant of encephalomyocarditis virus (EMC-D virus) showed lymphocytic infiltration with moderate to severe destruction of beta cells. Immunohistochemical staining of the islet sections with several monoclonal antibodies, anti-Mac-1, anti-Mac-2, and F4/80 for macrophages, anti-L3T4 for helper/inducer T cells, and anti-Lyt2 for cytotoxic/suppressor T cells revealed that the major population of infiltrating cells at the early stage of viral infection was Mac-2-positive macrophages. In contrast, macrophages detected by anti-Mac-1 and F4/80 monoclonal antibodies were not found at the early stage of viral infection but were found at intermediate and late stages of viral infection. Helper/inducer T cells and cytotoxic/suppressor T cells also infiltrated the islets at intermediate and late stages of viral infection. Short-term treatment of mice with silica prior to viral infection resulted in an enhancement of beta-cell destruction, leading to the development of diabetes. In contrast, long-term treatment of mice with silica resulted in complete prevention of diabetes caused by a low dose of viral infection and a significant decrease in the incidence of diabetes caused by an intermediate or high dose of viral infection. Furthermore, depletion of macrophages by a specific monoclonal antibody (anti-Mac-2) resulted in a much greater decrease in the incidence of diabetes caused by an intermediate dose of viral infection. However, suppression of helper/inducer T cells and cytotoxic/suppressor T cells, by anti-L3T4 and anti-Lyt2 antibodies, respectively, did not alter the incidence of diabetes. On the basis of these data, it is concluded that macrophages, particularly Mac-2-positive macrophages, play a crucial role in the process of pancreatic beta-cell destruction at the early stage of encephalomyocarditis D virus infection in SJL/J mice.</jats:p> |
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| spelling | Baek, H S Yoon, J W 0022-538X 1098-5514 American Society for Microbiology Virology Insect Science Immunology Microbiology http://dx.doi.org/10.1128/jvi.64.12.5708-5715.1990 <jats:p>Pancreatic islets from SJL/J mice infected with the D variant of encephalomyocarditis virus (EMC-D virus) showed lymphocytic infiltration with moderate to severe destruction of beta cells. Immunohistochemical staining of the islet sections with several monoclonal antibodies, anti-Mac-1, anti-Mac-2, and F4/80 for macrophages, anti-L3T4 for helper/inducer T cells, and anti-Lyt2 for cytotoxic/suppressor T cells revealed that the major population of infiltrating cells at the early stage of viral infection was Mac-2-positive macrophages. In contrast, macrophages detected by anti-Mac-1 and F4/80 monoclonal antibodies were not found at the early stage of viral infection but were found at intermediate and late stages of viral infection. Helper/inducer T cells and cytotoxic/suppressor T cells also infiltrated the islets at intermediate and late stages of viral infection. Short-term treatment of mice with silica prior to viral infection resulted in an enhancement of beta-cell destruction, leading to the development of diabetes. In contrast, long-term treatment of mice with silica resulted in complete prevention of diabetes caused by a low dose of viral infection and a significant decrease in the incidence of diabetes caused by an intermediate or high dose of viral infection. Furthermore, depletion of macrophages by a specific monoclonal antibody (anti-Mac-2) resulted in a much greater decrease in the incidence of diabetes caused by an intermediate dose of viral infection. However, suppression of helper/inducer T cells and cytotoxic/suppressor T cells, by anti-L3T4 and anti-Lyt2 antibodies, respectively, did not alter the incidence of diabetes. On the basis of these data, it is concluded that macrophages, particularly Mac-2-positive macrophages, play a crucial role in the process of pancreatic beta-cell destruction at the early stage of encephalomyocarditis D virus infection in SJL/J mice.</jats:p> Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice Journal of Virology |
| spellingShingle | Baek, H S, Yoon, J W, Journal of Virology, Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice, Virology, Insect Science, Immunology, Microbiology |
| title | Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_full | Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_fullStr | Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_full_unstemmed | Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_short | Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_sort | role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| title_unstemmed | Role of macrophages in the pathogenesis of encephalomyocarditis virus-induced diabetes in mice |
| topic | Virology, Insect Science, Immunology, Microbiology |
| url | http://dx.doi.org/10.1128/jvi.64.12.5708-5715.1990 |