南開(kāi)大學(xué)醫(yī)學(xué)院病理與免疫學(xué)系,，天津教育部生物活性物質(zhì)重點(diǎn)實(shí)驗(yàn)室的研究者在最新一期的Cancer Research上發(fā)布研究性文章。文章的通訊作者是南開(kāi)大學(xué)醫(yī)學(xué)院特聘教授楊榮存博士,。文章主要研究細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)抑制因子3（suppressor of cytokine Signaling 3,，簡(jiǎn)稱(chēng)SOCS3）對(duì)骨髓細(xì)胞分化的調(diào)控。
在白細(xì)胞介素6，脂多糖或是腫瘤相關(guān)因子的刺激下,，骨髓細(xì)胞（bone marrow cells,，BMC）中的細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)抑制因子3的表達(dá)量會(huì)上升。盡管這一現(xiàn)象已經(jīng)被發(fā)現(xiàn),，但是細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)抑制因子3的表達(dá)量增多對(duì)骨髓細(xì)胞的分化有什么影響,，這一問(wèn)題一直懸而未決。
在本研究中,，楊榮存教授帶領(lǐng)研究小組研究發(fā)現(xiàn)細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)抑制因子3的表達(dá)量上升可有效地促進(jìn)骨髓細(xì)胞單向分化成為CD8 T細(xì)胞,。更重要的是，肺可以成為一個(gè)無(wú)胸腺組織提供適應(yīng)的場(chǎng)所供骨髓細(xì)胞分化成CD8+T細(xì)胞,。在SOCS3促進(jìn)骨髓細(xì)胞分化成CD8+ T細(xì)胞過(guò)程中,，Notch1起關(guān)鍵的作用。因此,，研究者得出結(jié)論,，在某些病理?xiàng)l件（比如腫瘤，炎癥）下,，上調(diào)SOCS3的表達(dá)量可促進(jìn)肺組織中的Notch1表達(dá),，最終促進(jìn)骨髓細(xì)胞分化成為CD8+ T細(xì)胞。
這一結(jié)果為抗疾病尤其是抗腫瘤的理論增添了新內(nèi)容,。（生物谷Bioon.com）
生物谷推薦原始出處：
Cancer Research 69, 1578-1586, February 15, 2009.doi: 10.1158/0008-5472.CAN-08-2744
Suppressor of Cytokine Signaling 3 Promotes Bone Marrow Cells to Differentiate into CD8+ T Lymphocytes in Lung Tissue via Up-Regulating Notch1 Expression
Zhuohan Zhang1, Bin Zeng1, Zhiqian Zhang1, Guohui Jiao1, Haijie Li1, Zhizi Jing1, Jiangbo Ouyang1, Xin Yuan1, Limin Chai1, Yongzhe Che2, Yuan Zhang1 and Rongcun Yang1,3
Departments of 1 Immunology and 2 Pathology, Nankai University School of Medicine; 3 Key Laboratory of Bioactive Materials, Ministry of Education, Nankai University, Tianjin, People's Republic of China
Suppressor of cytokine signaling 3 (SOCS3) expression in bone marrow cells (BMC) was up-regulated upon exposure to interleukin 6, lipopolysaccharide, or tumor-associated factors. But, how the up-regulated SOCS3 affects differentiation of BMCs is incompletely characterized. Here, we showed that SOCS3 promoted BMCs to intently differentiate into CD8 T cells. Importantly, lung can be as one athymus tissue for the BMCs to differentiate into CD8+ T cells. Notch1 plays a critical role in the differentiation from SOCS3-transfected BMCs to CD8+ T cells. We conclude that the up-regulated SOCS3 in some pathologic conditions, such as tumor and inflammation, might promote BMCs to differentiate into CD8+ T lymphocytes in lung tissue via up-regulating Notch1 expression. This may represent a new mechanism against diseases such as tumor.
