医学方面的英译汉Negative Regulation of STATs by sacs Proteins in Sep

医学方面的英译汉
Negative Regulation of STATs by sacs Proteins in Sepsis and Septic Shock
The JAK/ST A T signal transduction pathway is negatively regulated by SOCS proteins DO,58J.Recent studies indicate that SOCS proteins are implicated in a variety of immune and inflammatory diseases [8].SOCSI-I- mice were highly sensitive to LPS-induced shock because of an increased serum level of TNF α [59,60].The introduction of SOCSI inhibited LPS-induced NF-ICB and STATl activation in macrophages.In addition,LPS tolerance,a refractory state to second LPS stimulation,was not observed in SOCSl mice [59,60].Thus,SOCSI negatively regulates LPS responses.Gene delivery of SOCS3 protected mice from lethal endotoxemia by decreasing the serum level of TNF α [61].These results suggest that SOCS1 and SOCS3 may be new targets for the treatment of endotoxin-induced shock syndrome that occasionally occurs following infection.
Very recently,we demonstrated that mice with a cell-specific overexpression of SOCS5 in T cells (SOCS5Tg) are resistant to the lethality relative to the WT mice [62J.The bacterial burden in SOCS5Tg mice was significantly lower than in WT mice,and the accumulation of leukocytes was augmented in SOCS5T g mice,which was accompanied by increased peritoneal levels of IL-12,IFN γ and TNF α
in vitro bactericidal activities of macrophages and neutrophils were enhanced in SOCS5Tg mice.Both neutrophils and macrophages from WT mice showed enhanced bacterial killing activity when co-cultured with CD4 + T cells from SOCS5Tg mice,relative to _D4 + T cells from WT mice.Furthermore,the :LP 嗣 induced bacterial burden in T - and B-cell-deficient RAG 去一 1- mice harboring SOCS5Tg-CD4 十 T ells was significantly reduced relative to the controls 62.These findings provide evidence that SOCS5 in T cells affects innate immunity,and thus they high- 19ht a novel role of T cells during sepsis.Further studies are necessary to elucidate the contribution of 、 cells to the initiation of innate immunity.

负调控的统计资料的囊中脓毒症和脓毒性休克蛋白
的JAK /意法半导体的AT信号转导通路是负面的溶解氧时SOCS蛋白,58J监管.最近的研究表明,在1时SOCS蛋白是免疫和炎症多种疾病有牵连[8].SOCSI - 1 -小鼠高度敏感LPS诱导因为有一个α肿瘤坏死因子[59,60]增加血清水平冲击.引进的SOCSI抑制脂多糖诱导的NF - ICB或STATl在巨噬细胞的活化.此外,内毒素耐受性,1至第二耐火材料国家LPS刺激,是不是在SOCSl小鼠[59,60]观察.因此,SOCSI负调控内毒素的反应.从致命的基因传递通过降低内毒素血症对肿瘤坏死因子α[61]血清水平SOCS3的保护小鼠.这些结果表明,SOCS1和SOCS3的可能是内毒素引起的休克症候群,偶尔会发生感染后治疗的新目标.
最近,我们证明了在T SOCS5细胞特异性表达小鼠细胞（SOCS5Tg）有抗药性的杀伤力相对于野生型小鼠[62J.在SOCS5Tg小鼠细菌负担显着高于野生型小鼠低,白细胞积聚在SOCS5T增强克小鼠,这是由白介素-12,干扰素γ和肿瘤坏死因子α水平的同时增加腹膜
巨噬细胞和中性粒细胞在体外杀菌活性增强SOCS5Tg小鼠.两个中性粒细胞和巨噬细胞WT小鼠显示细菌的杀伤活性增强合作时,与CD4 + T从SOCS5Tg小鼠,相对于_D4从野生型小鼠细胞+ T细胞的培养.此外,：唱片嗣细菌引起的负担,在T - 和B -细胞缺陷的鲁尔去一1 - 老鼠窝藏SOCS5Tg与CD4十Ŧ埃尔斯显着降低相对于对照组62.这些发现提供了证据表明,在T细胞的影响SOCS5先天免疫,因此,他们高19ht在败血症的T细胞的新角色.进一步的研究是必要的澄清的贡献,对先天免疫细胞开始.