L-Arginine modulates neonatal lymphocyte proliferation through an interleukin-2 independent pathway

Hong Ren Yu, Ho Chang Kuo, Li Tung Huang, Chih Cheng Chen, You Lin Tain, Jiunn Ming Sheen, Mao Meng Tiao, Hsin Chun Huang, Kuender D. Yang, Chia Yo Ou, Te Yao Hsu*

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

20 引文 斯高帕斯(Scopus)

摘要

Summary: In cases of arginine depletion, lymphocyte proliferation, cytokine production and CD3ζ chain expression are all diminished. In addition to myeloid suppressor cells, polymorphonuclear cells (PMN) also exert T-cell immune suppressive effects through arginase-induced l-arginine depletion, especially during pregnancy. In this study, we investigated how arginase/l-arginine modulates neonatal lymphocyte proliferation. Results showed that the neonatal plasma l-arginine level was lower than in adults (48·1 ± 11·3 versus 86·5 ± 14·6 μm; P = 0·003). Neonatal PMN had a greater abundance of arginase I protein than adult PMN. Both transcriptional regulation and post-transcriptional regulation were responsible for the higher arginase I expression of neonatal PMN. Exogenous l-arginine enhanced neonate lymphocyte proliferation but not that of adult cells. The RNA-binding protein HuR was important but was not the only modulation factor in l-arginine-regulated neonatal T-cell proliferation. l-Arginine-mediated neonatal lymphocyte proliferation could not be blocked by interleukin-2 receptor blocking antibodies. These results suggest that the altered arginase/l-arginine cascade may be one of the mechanisms that contribute to altered neonatal immune responses. Exogenous l-arginine could enhance neonate lymphocyte proliferation through an interleukin-2-independent pathway.

原文英語
頁(從 - 到)184-192
頁數9
期刊Immunology
143
發行號2
DOIs
出版狀態已出版 - 01 10 2014

文獻附註

Publisher Copyright:
© 2014 John Wiley & Sons Ltd.

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