英语翻译The animal model of multiple sclerosis,experimental autoimmuneencephalomyelitis (EAE),is induced by immunization withmyelin components or by adoptive transfer of encephalitogenicCD4+ T cells into naı¨ve animals (Zamvil and Steinman,

英语翻译The animal model of multiple sclerosis,experimental autoimmuneencephalomyelitis (EAE),is induced by immunization withmyelin components or by adoptive transfer of encephalitogenicCD4+ T cells into naı¨ve animals (Zamvil and Steinman,
英语翻译
The animal model of multiple sclerosis,experimental autoimmune
encephalomyelitis (EAE),is induced by immunization with
myelin components or by adoptive transfer of encephalitogenic
CD4+ T cells into naı¨ve animals (Zamvil and Steinman,1990).
Because of similarities to the EAE model,the fact that administration
of the quintessential T helper (Th) 1 cytokine gamma interferon
(IFN-g) worsened multiple sclerosis (Panitch et al.,1987),
and the typical cellular composition of brain- and cerebrospinal
fluid-infiltrating cells,multiple sclerosis for a long time was considered
to be a Th1-mediated disease (Sospedra and Martin,
2005).However,since the characterization of the Th17 phenotype
and its pathogenic role in EAE (Cua et al.,2003; Langrish et al.,
2005; Chen et al.,2006) and multiple sclerosis (Kebir et al.,2007),
there is ongoing debate whether Th1,Th17,or both subtypes of T
lymphocytes are important for the initiation of autoimmune CNS
inflammation (McFarland and Martin,2007; Steinman,2008).
Transforming growth factor (TGF)-b1 is a master regulator of
immune responses,initiating signalling events in target cells that
have vital and non-redundant regulatory functions (Letterio and
Roberts,1998; Li et al.,2006a).While TGF-b blocks the differentiation
of Th1 and Th2 cells by inhibiting T-bet and GATA-3(Gorelik et al.,2000,2002),respectively,it promotes the generation
of inducible regulatory T cells by up-regulating Foxp3 (Chen
et al.,2003).Under inflammatory conditions,in particular in the
presence of IL-6,TGF-b supports the differentiation of Th17 cells,
which are implicated in autoimmune diseases (Bettelli et al.,2006;
Mangan et al.,2006; Veldhoen et al.,2006).Despite rapid progress
in elucidating the cytokine networks involved in T cell differentiation,
molecular mechanisms mediating context-dependent
cellular responses after activation of the transforming growth
factor-b receptor (TGF-bR) are only partly understood.
The Smad family of proteins mediates signalling from the TGFbR
to the nucleus (Shi and Massague,2003).Smad7,which is
induced by TGFb itself,forms part of an inhibitory feedback-loop
by binding to the intracellular domain of the activated TGFbRI
(Hayashi et al.,1997; Nakao et al.,1997).It prevents the phosphorylation
of Smad proteins,associates with ubiquitin ligases
involved in TGF-bR-degradation and acts as a transcriptional
repressor inhibiting Smad-dependent promoter activation
(Schmierer and Hill,2007).Since Smad7 is responsible for the
fine-tuning of TGF-b signals (Itoh and ten Dijke,2007),an aberrant
expression of Smad7 might disrupt the balanced activity of
TGF-b under physiological and pathophysiological conditions.
生命科学方面，我自己翻译的题目名称是：T细胞中的Smad7促使多发性硬化症和实验性自身免疫脑脊髓炎中的Th1反应。

英语翻译The animal model of multiple sclerosis,experimental autoimmuneencephalomyelitis (EAE),is induced by immunization withmyelin components or by adoptive transfer of encephalitogenicCD4+ T cells into naı¨ve animals (Zamvil and Steinman,
自发的CD4+T淋巴细胞反应在多发性硬化症和它的动物模型以及实验性自身免疫脑脊炎(experimental autoimmune encephalomyelitis,EAE)的发病激励中发挥着重要的角色.自从Th17细胞发现以后,关于Th1、Th17或者所有T淋巴细胞的亚型是否对自身免疫神经炎症的引发起重要作用,科学届一直争论不休.Ingo Kleiter等检验了多发性复发缓解型硬化症病人的外周血CD4+细胞,并且用可以控制Smad7转化生长抑制因子缺失或过表达的小鼠来描述Smad7在T细胞分化和自身免疫性神经炎症中的角色.
多发性硬化症（multiple sclerosis）是中枢神经系统（CNS）的一种慢性炎症性和退行性疾病,这被认为是自身免疫疾病的源头.在大多数病人中,多发性硬发症最初表现为复发缓解型攻击中枢神经组织的急性炎症反应疾病,然后会完全康复.尽管多发性硬发怔的精确发病机制还不清楚,但髓鞘特异的CD4+T细胞的激活作用在神经炎症的引发中是中枢步骤,这是大家广泛接受的观点.多发性硬发症的最大遗传危险系数被发现实在HLA-DRA、IL-2R、IL-7R的基因中,特别强调CD4+T细胞的重要性.

？这个是人医还是兽医方面的内容？要的很急么