N- (2,4-Dinitrophenyl)-4-amino-n-butyl aldehyde 3 was obtained with high yield of 80% when N- (2,4-dinitrophenyl)-L-proline 1 reacted with SOCl2 at room temperature. However, the anticipated product N- (2,4-dinitroph...N- (2,4-Dinitrophenyl)-4-amino-n-butyl aldehyde 3 was obtained with high yield of 80% when N- (2,4-dinitrophenyl)-L-proline 1 reacted with SOCl2 at room temperature. However, the anticipated product N- (2,4-dinitrophenyl)-tetrahydropyrrolyl-2- (4-methylthiophenyl) ketone 2 did not be produced. The mechanism was discussed in this article.展开更多
Contact hypersensitivity(CHS)is a delayed-type hypersensitivity that can be induced by haptens,such as 2,4-dinitrofluorobenzene(DNFB).Innate and adaptive immunities are both important for the development of CHS.To tre...Contact hypersensitivity(CHS)is a delayed-type hypersensitivity that can be induced by haptens,such as 2,4-dinitrofluorobenzene(DNFB).Innate and adaptive immunities are both important for the development of CHS.To treat CHS-related diseases,such as allergic contact dermatitis,a disease prevalent in industrialized countries,ways of interfering with improper immune function during CHS responses need to be identified.Transforming growth factor-b-activated kinase-1(TAK1),a member of mitogen-activated protein kinase kinase kinase family,is important for both innate and adaptive immunities.We thus hypothesized that the CHS response could be inhibited by interfering with TAK1 activity.Using a mouse model in which TAK1 deletion can be locally induced,we observed that TAK deficiency led to an impaired CHS response and was associated with defective T-cell expansion,activation and interferon(IFN)-c production.In addition,we investigated the effect of deleting TAK1 specifically in dendritic cells(DC)on the CHS response.We found that when TAK1 is deficient in DC,the CHS response was abolished and hapten-elicited T-cell responses were defective.Collectively,this study demonstrates an essential role of TAK1 in the induction of CHS and suggests that targeting TAK1 could be a viable approach to treat CHS.展开更多
文摘N- (2,4-Dinitrophenyl)-4-amino-n-butyl aldehyde 3 was obtained with high yield of 80% when N- (2,4-dinitrophenyl)-L-proline 1 reacted with SOCl2 at room temperature. However, the anticipated product N- (2,4-dinitrophenyl)-tetrahydropyrrolyl-2- (4-methylthiophenyl) ketone 2 did not be produced. The mechanism was discussed in this article.
基金the National Institutes of Health(R00AI072956 to YYW)the Beijing Natural Science Foundation(7082054)the National Science and Technology Major Specific Project of the People’s Republic of China(2009ZX09301-010 to WH)and the China Scholarship Council(YGZ).
文摘Contact hypersensitivity(CHS)is a delayed-type hypersensitivity that can be induced by haptens,such as 2,4-dinitrofluorobenzene(DNFB).Innate and adaptive immunities are both important for the development of CHS.To treat CHS-related diseases,such as allergic contact dermatitis,a disease prevalent in industrialized countries,ways of interfering with improper immune function during CHS responses need to be identified.Transforming growth factor-b-activated kinase-1(TAK1),a member of mitogen-activated protein kinase kinase kinase family,is important for both innate and adaptive immunities.We thus hypothesized that the CHS response could be inhibited by interfering with TAK1 activity.Using a mouse model in which TAK1 deletion can be locally induced,we observed that TAK deficiency led to an impaired CHS response and was associated with defective T-cell expansion,activation and interferon(IFN)-c production.In addition,we investigated the effect of deleting TAK1 specifically in dendritic cells(DC)on the CHS response.We found that when TAK1 is deficient in DC,the CHS response was abolished and hapten-elicited T-cell responses were defective.Collectively,this study demonstrates an essential role of TAK1 in the induction of CHS and suggests that targeting TAK1 could be a viable approach to treat CHS.
