Xu Wang, Shuai Lu, Yankai Xiao, Ling Xu, Lingling Zhou, Junyan Hu, Bo Li, Chengwu Zeng, Yangqiu Li
{"title":"下调MALT1后CD3+ t细胞基因表达谱的改变。","authors":"Xu Wang, Shuai Lu, Yankai Xiao, Ling Xu, Lingling Zhou, Junyan Hu, Bo Li, Chengwu Zeng, Yangqiu Li","doi":"10.2147/ITT.S179656","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>T cell immunodeficiency is a common feature in patients with different kinds of hematological disease such as T cell non-Hodgkin lymphoma (T-NHL), B cells NHL (B-NHL), NK/T cell NHL (NK/T-CL) and acute myeloid leukemia (AML). In our recent research, we found that significantly lower expression levels in MALT1 and NF-κB were related to suppression of T cell activation. Therefore, this study was conducted to further investigate the role of downregulating MALT1 in the development of immunodeficiency in T cells.</p><p><strong>Methods: </strong>We induced activation inhibition in CD3<sup>+</sup> T cells by MALT1 knockdown. Then we characterized the gene expression profile after MALT1 suppression by microarray analysis.</p><p><strong>Result: </strong>The differentially expressed genes were <i>ZAP-70, p65, MDM2, ATM, NFATC2</i> which participate in the NF-κB, p53, and NFAT pathways in CD3<sup>+</sup> T cells after MALT1 downregulation.</p><p><strong>Conclusion: </strong>MALT1 suppression may contribute to immunodeficiency in T cells via suppression of T cell activation and proliferation pathways. These data may help to explain some of the characteristics of immunodeficiency of T cells.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"7 ","pages":"77-81"},"PeriodicalIF":6.2000,"publicationDate":"2018-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/ITT.S179656","citationCount":"0","resultStr":"{\"title\":\"Alteration of gene expression profile in CD3<sup>+</sup> T-cells after downregulating MALT1.\",\"authors\":\"Xu Wang, Shuai Lu, Yankai Xiao, Ling Xu, Lingling Zhou, Junyan Hu, Bo Li, Chengwu Zeng, Yangqiu Li\",\"doi\":\"10.2147/ITT.S179656\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>T cell immunodeficiency is a common feature in patients with different kinds of hematological disease such as T cell non-Hodgkin lymphoma (T-NHL), B cells NHL (B-NHL), NK/T cell NHL (NK/T-CL) and acute myeloid leukemia (AML). In our recent research, we found that significantly lower expression levels in MALT1 and NF-κB were related to suppression of T cell activation. Therefore, this study was conducted to further investigate the role of downregulating MALT1 in the development of immunodeficiency in T cells.</p><p><strong>Methods: </strong>We induced activation inhibition in CD3<sup>+</sup> T cells by MALT1 knockdown. Then we characterized the gene expression profile after MALT1 suppression by microarray analysis.</p><p><strong>Result: </strong>The differentially expressed genes were <i>ZAP-70, p65, MDM2, ATM, NFATC2</i> which participate in the NF-κB, p53, and NFAT pathways in CD3<sup>+</sup> T cells after MALT1 downregulation.</p><p><strong>Conclusion: </strong>MALT1 suppression may contribute to immunodeficiency in T cells via suppression of T cell activation and proliferation pathways. These data may help to explain some of the characteristics of immunodeficiency of T cells.</p>\",\"PeriodicalId\":30986,\"journal\":{\"name\":\"ImmunoTargets and Therapy\",\"volume\":\"7 \",\"pages\":\"77-81\"},\"PeriodicalIF\":6.2000,\"publicationDate\":\"2018-11-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.2147/ITT.S179656\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ImmunoTargets and Therapy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2147/ITT.S179656\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2018/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ImmunoTargets and Therapy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2147/ITT.S179656","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2018/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
Alteration of gene expression profile in CD3+ T-cells after downregulating MALT1.
Background: T cell immunodeficiency is a common feature in patients with different kinds of hematological disease such as T cell non-Hodgkin lymphoma (T-NHL), B cells NHL (B-NHL), NK/T cell NHL (NK/T-CL) and acute myeloid leukemia (AML). In our recent research, we found that significantly lower expression levels in MALT1 and NF-κB were related to suppression of T cell activation. Therefore, this study was conducted to further investigate the role of downregulating MALT1 in the development of immunodeficiency in T cells.
Methods: We induced activation inhibition in CD3+ T cells by MALT1 knockdown. Then we characterized the gene expression profile after MALT1 suppression by microarray analysis.
Result: The differentially expressed genes were ZAP-70, p65, MDM2, ATM, NFATC2 which participate in the NF-κB, p53, and NFAT pathways in CD3+ T cells after MALT1 downregulation.
Conclusion: MALT1 suppression may contribute to immunodeficiency in T cells via suppression of T cell activation and proliferation pathways. These data may help to explain some of the characteristics of immunodeficiency of T cells.
期刊介绍:
Immuno Targets and Therapy is an international, peer-reviewed open access journal focusing on the immunological basis of diseases, potential targets for immune based therapy and treatment protocols employed to improve patient management. Basic immunology and physiology of the immune system in health, and disease will be also covered.In addition, the journal will focus on the impact of management programs and new therapeutic agents and protocols on patient perspectives such as quality of life, adherence and satisfaction.