南開大學醫(yī)學院病理與免疫學系，天津教育部生物活性物質(zhì)重點實驗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大學醫(yī)學院特聘教授楊榮存博士,。文章主要研究細胞因子信號轉(zhuǎn)導抑制因子3（suppressor of cytokine Signaling 3，簡稱SOCS3）對骨髓細胞分化的調(diào)控,。
在白細胞介素6,，脂多糖或是腫瘤相關(guān)因子的刺激下，骨髓細胞（bone marrow cells,，BMC）中的細胞因子信號轉(zhuǎn)導抑制因子3的表達量會上升,。盡管這一現(xiàn)象已經(jīng)被發(fā)現(xiàn)，但是細胞因子信號轉(zhuǎn)導抑制因子3的表達量增多對骨髓細胞的分化有什么影響,，這一問題一直懸而未決,。
在本研究中，楊榮存教授帶領(lǐng)研究小組研究發(fā)現(xiàn)細胞因子信號轉(zhuǎn)導抑制因子3的表達量上升可有效地促進骨髓細胞單向分化成為CD8 T細胞,。更重要的是,，肺可以成為一個無胸腺組織提供適應的場所供骨髓細胞分化成CD8+T細胞。在SOCS3促進骨髓細胞分化成CD8+ T細胞過程中,，Notch1起關(guān)鍵的作用,。因此，研究者得出結(jié)論,，在某些病理條件（比如腫瘤,，炎癥）下，上調(diào)SOCS3的表達量可促進肺組織中的Notch1表達,，最終促進骨髓細胞分化成為CD8+ T細胞,。
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.
