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Double negative T cells mediate Lag3-dependent antigen-specific protection in allergic asthma

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单位: [1]General Surgery Department, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China [2]Experimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China [3]Beijing Clinical Research Institute, Beijing 100050, China [4]Beijing Key Laboratory of Tolerance Induction and Organ Protection in Transplantation, Beijing 100050, China [5]National Clinical Research Center for Digestive Diseases, Beijing 100050, China.
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Allergic asthma is an inflammatory disorder of the airway without satisfactory traditional therapies capable of controlling the underlying pathology. New approaches that can overcome the detrimental effects of immune dysregulation are thus desirable. Here we adoptively transfer ovalbumin (OVA) peptide-primed CD4(-) CD8(-) double negative T (DNT) cells intravenously into a mouse model of OVA-induced allergic asthma to find that OVA-induced airway hyperresponsiveness, lung inflammation, mucus production and OVA-specific IgG/IgE production are significantly suppressed. The immunosuppressive function of the OVA-specific DNT cells is dependent on the inhibition of CD11b+ dendritic cell function, T follicular helper cell proliferation, and IL-21 production. Mechanistically, Lag3 contributes to MHC-II antigen recognition and trogocytosis, thereby modulating the antigen-specific immune regulation by DNT cells. The effectiveness of ex vivo-generated allergen-specific DNT cells in alleviating airway inflammation thus supports the potential utilization of DNT cell-based therapy for the treatment of allergic asthma.

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出版当年[2018]版:
大类 | 2 区 综合性期刊
小类 | 2 区 综合性期刊
最新[2025]版:
大类 | 1 区 综合性期刊
小类 | 1 区 综合性期刊
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出版当年[2017]版:
Q1 MULTIDISCIPLINARY SCIENCES
最新[2023]版:
Q1 MULTIDISCIPLINARY SCIENCES

影响因子: 最新[2023版] 最新五年平均[2021-2025] 出版当年[2017版] 出版当年五年平均[2013-2017] 出版前一年[2016版] 出版后一年[2018版]

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第一作者单位: [1]General Surgery Department, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China [2]Experimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China [3]Beijing Clinical Research Institute, Beijing 100050, China [4]Beijing Key Laboratory of Tolerance Induction and Organ Protection in Transplantation, Beijing 100050, China
通讯作者:
通讯机构: [1]General Surgery Department, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China [2]Experimental and Translational Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China [3]Beijing Clinical Research Institute, Beijing 100050, China [4]Beijing Key Laboratory of Tolerance Induction and Organ Protection in Transplantation, Beijing 100050, China [5]National Clinical Research Center for Digestive Diseases, Beijing 100050, China.
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