近日,，日本一個研究小組在利用小鼠進行的實驗中發(fā)現(xiàn),，肺部大量存在的一種細胞，在持續(xù)產(chǎn)生導致過敏癥的蛋白質(zhì)的同時,，也具備遏制癌細胞轉(zhuǎn)移的作用,。

富山大學研究生院等機構(gòu)的研究人員日前在《免疫學雜志》上報告說，如果能夠弄清這種細胞的“雙刃劍”機制，并且加以利用,，人們就能更好地治療過敏癥和癌癥,。

醫(yī)學界認為，嗜酸性粒細胞在人體內(nèi)的增殖和活躍是引發(fā)過敏性哮喘和特應(yīng)癥等過敏癥的原因之一,。此前的研究顯示,，免疫系統(tǒng)中的淋巴T細胞產(chǎn)生的白介素－5能促使嗜酸性粒細胞活躍。

而在新的實驗中,，日本研究人員發(fā)現(xiàn),，小鼠肺部和腸道存在的一種細胞能比淋巴T細胞產(chǎn)生更多的白介素－5。他們將這種細胞命名為“原始白介素－5產(chǎn)生細胞”,。今后如果能夠找到遏制這種細胞活動的方法,，就有可能開發(fā)出治療過敏性哮喘等過敏癥的方法。(生物谷 Bioon.com)

doi:10.4049/jimmunol.1101270
PMC:
PMID:
Identification of Innate IL-5–Producing Cells and Their Role in Lung Eosinophil Regulation and Antitumor Immunity

Masashi Ikutani, Tsutomu Yanagibashi, Masaru Ogasawara, Koichi Tsuneyama, Seiji Yamamoto, Yuichi Hattori, Taku Kouro, Atsuko Itakura, Yoshinori Nagai, Satoshi Takaki, and Kiyoshi Takatsu

內(nèi)容Transcriptional coregulators control the activity of many transcription factors and are thought to have wide- ranging effects on gene expression patterns. We show here that muscle-specific loss of nuclear receptor corepressor 1 (NCoR1) in mice leads to enhanced exercise endurance due to an increase of both muscle mass and of mitochondrial number and activity. The activation of selected transcription factors that control muscle function, such as MEF2, PPARβ/, and ERRs, underpins these phenotypic alterations. NCoR1 levels are decreased in conditions that require fat oxidation, resetting transcriptional programs to boost oxidative metabolism. Knockdown of gei-8, the sole C. elegans NCoR homolog, also robustly increased muscle mitochondria and respiration, suggesting conservation of NCoR1 function. Collectively, our data suggest that NCoR1 plays an adaptive role in muscle physiology and that interference with NCoR1 action could be used to improve muscle function.