问题描述:
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。
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。
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