Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice.
Epstein-Barr virus-induced gene-3 (EBI-3) associates with p28 to form interleukin-27 (IL-27) or with IL-12p35 to form IL-35. Both IL-27 and IL-35 have immunosuppressive functions and especially IL-35 has been implicated in the suppressive function of regulatory T cells (Treg). To address the role of...
Autori principali: | , , , , , , |
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Natura: | Journal article |
Lingua: | English |
Pubblicazione: |
2010
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_version_ | 1826292945059315712 |
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author | Tong, H Miyazaki, Y Yamazaki, M Hara, H Waldmann, H Hori, S Yoshida, H |
author_facet | Tong, H Miyazaki, Y Yamazaki, M Hara, H Waldmann, H Hori, S Yoshida, H |
author_sort | Tong, H |
collection | OXFORD |
description | Epstein-Barr virus-induced gene-3 (EBI-3) associates with p28 to form interleukin-27 (IL-27) or with IL-12p35 to form IL-35. Both IL-27 and IL-35 have immunosuppressive functions and especially IL-35 has been implicated in the suppressive function of regulatory T cells (Treg). To address the role of EBI-3 in immune regulation, delayed-type hypersensitivity (DTH) responses were examined in EBI-3-deficient (EBI-3(-/-)) mice. EBI-3(-/-) mice developed deteriorated DTH responses as shown by the enhanced footpad swelling and augmented infiltration of inflammatory cells into the antigen-challenged footpads as compared with wild-type (WT) mice. While EBI-3-deficiency showed little effects on antigen-specific IFN-gamma production of lymph node cells, IL-17 production was drastically augmented in EBI-3(-/-) cells as compared with in WT cells. In addition, reduced IL-10 production was also evident in EBI-3(-/-) CD4(+) T cells. Interestingly, the development and suppressive function of Treg to inhibit effector T cell proliferation was not affected by EBI-3-deficiency. These data clearly demonstrated the immunosuppressive function of EBI-3 and provided complementary evidence that EBI-3 and EBI-3-containing cytokines might be taken into consideration as potential targets for some immune-related diseases. |
first_indexed | 2024-03-07T03:22:30Z |
format | Journal article |
id | oxford-uuid:b7e688c1-f437-4c48-b719-383076f9ac70 |
institution | University of Oxford |
language | English |
last_indexed | 2024-03-07T03:22:30Z |
publishDate | 2010 |
record_format | dspace |
spelling | oxford-uuid:b7e688c1-f437-4c48-b719-383076f9ac702022-03-27T04:52:07ZExacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:b7e688c1-f437-4c48-b719-383076f9ac70EnglishSymplectic Elements at Oxford2010Tong, HMiyazaki, YYamazaki, MHara, HWaldmann, HHori, SYoshida, HEpstein-Barr virus-induced gene-3 (EBI-3) associates with p28 to form interleukin-27 (IL-27) or with IL-12p35 to form IL-35. Both IL-27 and IL-35 have immunosuppressive functions and especially IL-35 has been implicated in the suppressive function of regulatory T cells (Treg). To address the role of EBI-3 in immune regulation, delayed-type hypersensitivity (DTH) responses were examined in EBI-3-deficient (EBI-3(-/-)) mice. EBI-3(-/-) mice developed deteriorated DTH responses as shown by the enhanced footpad swelling and augmented infiltration of inflammatory cells into the antigen-challenged footpads as compared with wild-type (WT) mice. While EBI-3-deficiency showed little effects on antigen-specific IFN-gamma production of lymph node cells, IL-17 production was drastically augmented in EBI-3(-/-) cells as compared with in WT cells. In addition, reduced IL-10 production was also evident in EBI-3(-/-) CD4(+) T cells. Interestingly, the development and suppressive function of Treg to inhibit effector T cell proliferation was not affected by EBI-3-deficiency. These data clearly demonstrated the immunosuppressive function of EBI-3 and provided complementary evidence that EBI-3 and EBI-3-containing cytokines might be taken into consideration as potential targets for some immune-related diseases. |
spellingShingle | Tong, H Miyazaki, Y Yamazaki, M Hara, H Waldmann, H Hori, S Yoshida, H Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. |
title | Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. |
title_full | Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. |
title_fullStr | Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. |
title_full_unstemmed | Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. |
title_short | Exacerbation of delayed-type hypersensitivity responses in EBV-induced gene-3 (EBI-3)-deficient mice. |
title_sort | exacerbation of delayed type hypersensitivity responses in ebv induced gene 3 ebi 3 deficient mice |
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