目的探讨LAT和CD99在T淋巴母细胞淋巴瘤(precursor T lymphoblastic lymphoma,T-LBL)中表达的价值。方法对37例T-LBL应用免疫组织化学EnVision二步法进行LAT和CD99标记。同时选取15例其他病例作为对照:3例B淋巴母细胞淋巴瘤,4例非特殊...目的探讨LAT和CD99在T淋巴母细胞淋巴瘤(precursor T lymphoblastic lymphoma,T-LBL)中表达的价值。方法对37例T-LBL应用免疫组织化学EnVision二步法进行LAT和CD99标记。同时选取15例其他病例作为对照:3例B淋巴母细胞淋巴瘤,4例非特殊类型外周T细胞淋巴瘤,3例结外鼻型NK/T细胞淋巴瘤,5例淋巴结反应性增生。结果37例T-LBL均表达LAT和CD99;4例外周T细胞淋巴瘤及3例鼻型结外NK/T细胞淋巴瘤弥漫表达LAT,不表达CD99;3例B淋巴母细胞淋巴瘤均表达CD99,但不表达LAT;5例反应性增生淋巴结的T细胞区LAT阳性,淋巴结皮、髓质区均不表达CD99。结论联合检测LAT和CD99有助于T-LBL的诊断和鉴别诊断。展开更多
Background Allergic asthma is associated with airway inflammation and hyperresponsiveness caused by dysregulated production of cytokines secreted by allergen-specific helper T-type 2 （Th2） cells. The linker for acti...Background Allergic asthma is associated with airway inflammation and hyperresponsiveness caused by dysregulated production of cytokines secreted by allergen-specific helper T-type 2 （Th2） cells. The linker for activation of T cells （LAT） is a membrane-associated adaptor protein, which has been shown to take part in regulating T cell receptor （TCR） signaling and T cell homeostasis. In this study, we established an asthmatic mouse model to examine the changes in LAT levels during allergic airway disease and the effects of LAT transgenic expression on airway inflammation. Methods T cells from mouse lung tissues were isolated from allergen challenged （ovalbumin （OVA）） and control mice, and the purity of these isolated T cells was examined by fluorescence-activated cell sorter （FACS）. Semi-quantitative RT-PCR and Western blotting were used to detect the expression of the LAT gene and LAT protein, respectively. After an intranasally administered mixture of pCMV-HA-LAT plasmid and Lipofectamine 2000, 24 hours before and 72 hours after allergen challenge, the BALF cell count and the differential cytologies were studied. In addition, IL-4 and IFN-γ levels in the BALF were determined by ELISA, and pathological changes in lung tissues were observed. Results LAT protein and mRNA expression were decreased in lung T cells in a mouse model of allergen-induced airway disease. After intranasal administration of pCMV-HA-LAT, histopathological examination of the lungs showed that intervention with LAT overexpression prevented mice from developing airway inflammation, and the number of total cells, eosinophils, neutrophils, and lymphocytes in the BALF was reduced significantly compared with the OVA sensitized and challenged group. In addition, the Th2 cytokine IL-4 decreased, while the Thl cytokine IFN-γ increased compared to the OVA sensitized and challenged group or the OVA sensitized group plus pCMV-HA treatment. Conclusion This study demonstrates that LAT might effectively diminish Th2 cytokine responses, lung histopathological changes and lung inflammation to allergen challenge in a model of expedmentally induced asthma.展开更多
文摘目的探讨LAT和CD99在T淋巴母细胞淋巴瘤(precursor T lymphoblastic lymphoma,T-LBL)中表达的价值。方法对37例T-LBL应用免疫组织化学EnVision二步法进行LAT和CD99标记。同时选取15例其他病例作为对照:3例B淋巴母细胞淋巴瘤,4例非特殊类型外周T细胞淋巴瘤,3例结外鼻型NK/T细胞淋巴瘤,5例淋巴结反应性增生。结果37例T-LBL均表达LAT和CD99;4例外周T细胞淋巴瘤及3例鼻型结外NK/T细胞淋巴瘤弥漫表达LAT,不表达CD99;3例B淋巴母细胞淋巴瘤均表达CD99,但不表达LAT;5例反应性增生淋巴结的T细胞区LAT阳性,淋巴结皮、髓质区均不表达CD99。结论联合检测LAT和CD99有助于T-LBL的诊断和鉴别诊断。
基金This work was supported by the Key Program of Shanghai Natural Science Foundation （No. 04JC14048）.Acknowledgments： We are grateful to Dr. Kevin S. Harrod （Lovelace Respiratory Research Institute, NM, USA） for critical reading of this manuscript and helpful suggestion and discussion.
文摘Background Allergic asthma is associated with airway inflammation and hyperresponsiveness caused by dysregulated production of cytokines secreted by allergen-specific helper T-type 2 （Th2） cells. The linker for activation of T cells （LAT） is a membrane-associated adaptor protein, which has been shown to take part in regulating T cell receptor （TCR） signaling and T cell homeostasis. In this study, we established an asthmatic mouse model to examine the changes in LAT levels during allergic airway disease and the effects of LAT transgenic expression on airway inflammation. Methods T cells from mouse lung tissues were isolated from allergen challenged （ovalbumin （OVA）） and control mice, and the purity of these isolated T cells was examined by fluorescence-activated cell sorter （FACS）. Semi-quantitative RT-PCR and Western blotting were used to detect the expression of the LAT gene and LAT protein, respectively. After an intranasally administered mixture of pCMV-HA-LAT plasmid and Lipofectamine 2000, 24 hours before and 72 hours after allergen challenge, the BALF cell count and the differential cytologies were studied. In addition, IL-4 and IFN-γ levels in the BALF were determined by ELISA, and pathological changes in lung tissues were observed. Results LAT protein and mRNA expression were decreased in lung T cells in a mouse model of allergen-induced airway disease. After intranasal administration of pCMV-HA-LAT, histopathological examination of the lungs showed that intervention with LAT overexpression prevented mice from developing airway inflammation, and the number of total cells, eosinophils, neutrophils, and lymphocytes in the BALF was reduced significantly compared with the OVA sensitized and challenged group. In addition, the Th2 cytokine IL-4 decreased, while the Thl cytokine IFN-γ increased compared to the OVA sensitized and challenged group or the OVA sensitized group plus pCMV-HA treatment. Conclusion This study demonstrates that LAT might effectively diminish Th2 cytokine responses, lung histopathological changes and lung inflammation to allergen challenge in a model of expedmentally induced asthma.
