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Park, Jung Won,Min, Hyun Jung,Sohn, Jung Ho,Kim, Joo Young,Hong, Jeong Ho,Sigrist, Kirsten S.,Glimcher, Laurie H.,Hwang, Eun Sook Elsevier 2009 The journal of allergy and clinical immunology Vol.123 No.2
<P><B>Background</B></P><P>A T<SUB>H</SUB>1-specific transcription factor, T-box–containing protein expressed in T cells (T-bet), controls the production of both T<SUB>H</SUB>1 and T<SUB>H</SUB>2 cytokines in T<SUB>H</SUB> cell differentiation by means of distinct mechanisms. T-bet–deficient mice overproduce T<SUB>H</SUB>2 cytokines and have spontaneous airway inflammation.</P><P><B>Objectives</B></P><P>We tested whether T-bet overexpression could protect against the development or progression of asthma.</P><P><B>Methods</B></P><P>We generated a T cell–specific and inducible line of T-bet–transgenic mice on a T-bet–deficient genetic background and used it to study the function of T-bet in an ovalbumin (OVA)–induced asthma model.</P><P><B>Results</B></P><P>Induction of T-bet in a T cell–specific manner in an OVA model of asthma concomitant with OVA injection prevented airway hyperresponsiveness, eosinophilic and lymphocytic inflammation, and IL-5 and IL-13 production in bronchoalveolar lavage fluid and also reduced serum IgE and T<SUB>H</SUB>2 cytokine production by peripheral T cells. Even when T-bet expression was induced during later stages of asthma progression, T-bet overexpression still attenuated airway hyperresponsiveness and goblet cell hyperplasia, as well as T<SUB>H</SUB>2 cytokine production.</P><P><B>Conclusions</B></P><P>Our results suggest that T-bet expression in T cells can prevent the initiation of airway inflammation and progression of chronic inflammation and might be extrapolated to human asthma.</P>
Restoration ofT-box-containing protein expressed in T cells protects against allergen-induced asthma
Eun Sook, Hwang,Jung Won, Park,Hyun Jung, Min,Jung Ho, Sohn,Joo Young, Kim,Jeong Ho, Hong,Kirsten S. Sigrist,Laurie H. Glimcher 이화여자대학교 약학연구소 2010 藥學硏究論文集 Vol.- No.20
BACKGROUND: A T(H)1-specific transcription factor, T-box-containing protein expressed in T cells (T-bet), controls the production of both T(H)1 and T(H)2 cytokines in T(H) cell differentiation by means of distinct mechanisms. T-bet-deficient mice overproduce T(H)2 cytokines and have spontaneous airway inflammation. OBJECTIVES: We tested whether T-bet overexpression could protect against the development or progression of asthma. METHODS: We generated a T cell-specific and inducible line of T-bet-transgenic mice on a T-bet-deficient genetic background and used it to study the function of T-bet in an ovalbumin (OVA)-induced asthma model. RESULTS: Induction of T-bet in a T cell-specific manner in an OVA model of asthma concomitant with OVA injection prevented airway hyperresponsiveness, eosinophilic and lymphocytic inflammation, and IL-5 and IL-13 production in bronchoalveolar lavage fluid and also reduced serum IgE and T(H)2 cytokine production by peripheral T cells. Even when T-bet expression was induced during later stages of asthma progression, T-bet overexpression still attenuated airway hyperresponsiveness and goblet cell hyperplasia, as well as T(H)2 cytokine production. CONCLUSIONS: Our results suggest that T-bet expression in T cells can prevent the initiation of airway inflammation and progression of chronic inflammation and might be extrapolated to human asthma.