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Interleukin-27-Producing CD4+ T Cells Regulate Protective Immunity during Malaria Parasite Infection

発表形態:
原著論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2016年03月
DOI:
10.1016/j.immuni.2016.02.011
会議属性:
指定なし
査読:
有り
リンク情報:

日本語フィールド

著者:
Daisuke Kimura, Mana Miyakoda, Kazumi Kimura, Kiri Honma, Hiromitsu Hara, Hiroki Yoshida, Katsuyuki Yui
題名:
Interleukin-27-Producing CD4+ T Cells Regulate Protective Immunity during Malaria Parasite Infection
発表情報:
Immunity. 巻: 44 号: 3 ページ: 672-82.
キーワード:
概要:
Interleukin-27 (IL-27) is a heterodimeric regulatory cytokine of the IL-12 family, which is produced by macrophages, dendritic cells, and B cells upon stimulation through innate immune receptors. Here, we described regulatory CD4+ T cells that produce IL-27 in response to T cell receptor stimu- lation during malaria infection, inhibiting IL-2 pro- duction and clonal expansion of other T cells in an IL-27-dependent manner. IL-27-producing CD4+ T cells were Foxp3 CD11a+CD49d+ malaria antigen-specific CD4+ T cells and were distinct from interferon-g (IFN-g) producing Th1 or IL-10 producing Tr1 cells. In mice lacking IL-27 in T cells, IL-2 production was restored and clonal expansion and IFN-g production by specific CD4+ T cells were improved, culminating in reduced parasite burden. This study highlights a unique population of IL-27 producing regulatory CD4+ T cells and their critical role in the regulation of the protective immune response against malaria parasites.
抄録:
Interleukin-27 (IL-27) is a heterodimeric regulatory cytokine of the IL-12 family, which is produced by macrophages, dendritic cells, and B cells upon stimulation through innate immune receptors. Here, we described regulatory CD4+ T cells that produce IL-27 in response to T cell receptor stimu- lation during malaria infection, inhibiting IL-2 pro- duction and clonal expansion of other T cells in an IL-27-dependent manner. IL-27-producing CD4+ T cells were Foxp3 CD11a+CD49d+ malaria antigen-specific CD4+ T cells and were distinct from interferon-g (IFN-g) producing Th1 or IL-10 producing Tr1 cells. In mice lacking IL-27 in T cells, IL-2 production was restored and clonal expansion and IFN-g production by specific CD4+ T cells were improved, culminating in reduced parasite burden. This study highlights a unique population of IL-27 producing regulatory CD4+ T cells and their critical role in the regulation of the protective immune response against malaria parasites.

英語フィールド

Author:
Daisuke Kimura, Mana Miyakoda, Kazumi Kimura, Kiri Honma, Hiromitsu Hara, Hiroki Yoshida, Katsuyuki Yui
Title:
Interleukin-27-Producing CD4+ T Cells Regulate Protective Immunity during Malaria Parasite Infection
Announcement information:
Immunity. Vol: 44 Issue: 3 Page: 672-82.
An abstract:
Interleukin-27 (IL-27) is a heterodimeric regulatory cytokine of the IL-12 family, which is produced by macrophages, dendritic cells, and B cells upon stimulation through innate immune receptors. Here, we described regulatory CD4+ T cells that produce IL-27 in response to T cell receptor stimu- lation during malaria infection, inhibiting IL-2 pro- duction and clonal expansion of other T cells in an IL-27-dependent manner. IL-27-producing CD4+ T cells were Foxp3 CD11a+CD49d+ malaria antigen-specific CD4+ T cells and were distinct from interferon-g (IFN-g) producing Th1 or IL-10 producing Tr1 cells. In mice lacking IL-27 in T cells, IL-2 production was restored and clonal expansion and IFN-g production by specific CD4+ T cells were improved, culminating in reduced parasite burden. This study highlights a unique population of IL-27 producing regulatory CD4+ T cells and their critical role in the regulation of the protective immune response against malaria parasites.
An abstract:
Interleukin-27 (IL-27) is a heterodimeric regulatory cytokine of the IL-12 family, which is produced by macrophages, dendritic cells, and B cells upon stimulation through innate immune receptors. Here, we described regulatory CD4+ T cells that produce IL-27 in response to T cell receptor stimu- lation during malaria infection, inhibiting IL-2 pro- duction and clonal expansion of other T cells in an IL-27-dependent manner. IL-27-producing CD4+ T cells were Foxp3 CD11a+CD49d+ malaria antigen-specific CD4+ T cells and were distinct from interferon-g (IFN-g) producing Th1 or IL-10 producing Tr1 cells. In mice lacking IL-27 in T cells, IL-2 production was restored and clonal expansion and IFN-g production by specific CD4+ T cells were improved, culminating in reduced parasite burden. This study highlights a unique population of IL-27 producing regulatory CD4+ T cells and their critical role in the regulation of the protective immune response against malaria parasites.


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