ID | 114921 |
タイトル別表記 | CD98 and T Cell Activation
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著者 |
Kurihara, Takeshi
Tokushima University
Bhuyan, Zaied Ahmed
Tokushima University
Tsumura, Hideki
National Research Institute for Child Health and Development
Ito, Morihiro
Chubu University
Ito, Yasuhiko
Chubu University
前川, 洋一
Tokushima University
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資料タイプ |
学術雑誌論文
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抄録 | Upon their recognition of antigens presented by the MHC, T cell proliferation is vital for clonal expansion and the acquisition of effector functions, which are essential for mounting adaptive immune responses. The CD98 heavy chain (CD98hc, Slc3a2) plays a crucial role in the proliferation of both CD4+ and CD8+ T cells, although it is unclear if CD98hc directly regulates the T cell effector functions that are not linked with T cell proliferation in vivo. Here, we demonstrate that CD98hc is required for both CD4+ T cell proliferation and Th1 functional differentiation. T cell-specific deletion of CD98hc did not affect T cell development in the thymus. CD98hc-deficient CD4+ T cells proliferated in vivo more slowly as compared with control T cells. C57BL/6 mice lacking CD98hc in their CD4+ T cells could not control Leishmania major infections due to lowered IFN-γ production, even with massive CD4+ T cell proliferation. CD98hc-deficient CD4+ T cells exhibited lower IFN-γ production compared with wild-type T cells, even when comparing IFN-γ expression in cells that underwent the same number of cell divisions. Therefore, these data indicate that CD98hc is required for CD4+ T cell expansion and functional Th1 differentiation in vivo, and suggest that CD98hc might be a good target for treating Th1-mediated immune disorders.
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掲載誌名 |
PLOS ONE
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ISSN | 19326203
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出版者 | PLOS
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巻 | 10
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号 | 10
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開始ページ | e0139692
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発行日 | 2015-10-07
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権利情報 | © 2015 Kurihara et al. This is an open access article distributed under the terms of the Creative Commons Attribution License(https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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言語 |
eng
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出版社版
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部局 |
医学系
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