Interleukin-7 Receptor is Indispensable for Proliferation and Survival in Thymic γδT Cell Development
Background: Interleukin-7 receptor (IL-7R) α-deficient mice have small numbers of B cells and αβT cells in periphery, they totally lack γδT cells. In addition, the V-J recombination and transcription of TCRγ genes is also severely impaired in IL-7Rα-deficient mice. Stat5, a signaling molecule of the...
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Published in | Immune network Vol. 5; no. 1; pp. 23 - 29 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
대한면역학회
2005
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Subjects | |
Online Access | Get full text |
ISSN | 1598-2629 2092-6685 |
DOI | 10.4110/in.2005.5.1.23 |
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Summary: | Background: Interleukin-7 receptor (IL-7R) α-deficient mice have small numbers of B cells and αβT cells in periphery, they totally lack γδT cells. In addition, the V-J recombination and transcription of TCRγ genes is also severely impaired in IL-7Rα-deficient mice. Stat5, a signaling molecule of the IL-7R, induces germline transcription in the TCRγ locus, and promotes V-J recombination and γδT cell development. However, the roles for IL-7R signaling pathway in thymic or extrathymic γδT cell development are largely unknown. Methods: To clarify the role of the IL-7 receptor in proliferation and survival of γδT cells, we introduced the TCR γδ transgene, Vγ2/ Vδ5, into IL-7Rα-deficient mice, and investigated the development of γδT cells. Results: We found that Vγ2/Vδ5 transgene restored γδT cells in the epithelium of the small intestine (IEL) but not in the thymus and the spleen. Further addition of a bcl-2 transgene resulted in partial recovery of γδT cells in the thymus and the spleen of these mice. Conclusion: Taken together, this study revealed that the IL-7Rα is indispensable for proliferation and survival mainly in thymic γδT cell development. KCI Citation Count: 0 |
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Bibliography: | G704-001562.2005.5.1.005 http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0923620050050010023 |
ISSN: | 1598-2629 2092-6685 |
DOI: | 10.4110/in.2005.5.1.23 |