نمایش مختصر رکورد

dc.contributor.authorLiu, Yonganen_US
dc.contributor.authorNie, Weien_US
dc.contributor.authorJin, Yuen_US
dc.contributor.authorZhuo, Anshanen_US
dc.contributor.authorZang, Yuanshengen_US
dc.contributor.authorXiu, Qingyuen_US
dc.date.accessioned1399-07-09T07:48:36Zfa_IR
dc.date.accessioned2020-09-30T07:48:36Z
dc.date.available1399-07-09T07:48:36Zfa_IR
dc.date.available2020-09-30T07:48:36Z
dc.date.issued2016-06-01en_US
dc.date.issued1395-03-12fa_IR
dc.date.submitted2016-08-02en_US
dc.date.submitted1395-05-12fa_IR
dc.identifier.citationLiu, Yongan, Nie, Wei, Jin, Yu, Zhuo, Anshan, Zang, Yuansheng, Xiu, Qingyu. (2016). B and T Lymphocyte Attenuator is a Target of miR-155 during Naive CD4+ T Cell Activation. Iranian Journal of Immunology, 13(2), 89-99.en_US
dc.identifier.issn1735-1383
dc.identifier.issn1735-367X
dc.identifier.urihttps://iji.sums.ac.ir/article_16660.html
dc.identifier.urihttps://iranjournals.nlai.ir/handle/123456789/329320
dc.description.abstract<strong>Background</strong>: MicroRNA-155 (miR-155) is upregulated during T cell activation, but the exact mechanisms by which it influences CD4+ T cell activation remain unclear. <br/><strong>Objective</strong>: To examine whether the B and T lymphocyte attenuator (BTLA) is a target of miR-155 during naïve CD4+ T cell activation. Methods: Firefly luciferase reporter plasmids pEZX-MT01-wild-type-BTLA and pEZX-MT01-mutant-BTLA were constructed. Lymphocytes were nucleofected with miR-155 inhibitor or negative control (NC). Then, naïve CD4+ CD62L+ helper T cells purified from lymphocytes were stimulated with immobilized antibody to CD3 and soluble antibody to CD28. miR-155 and BTLA expression were examined by real-time RT-PCR. Cell surface CD69 expression and IL-2 secretion were measured by ELISA and flowcytometry, respectively. <br/><strong>Results</strong>: Luciferase reporter assay showed that miR-155 targeted the BTLA 3'UTR region. Compared with non-stimulated condition, both miR-155 and BTLA mRNA expression were upregulated after T cell activation. Similar results were observed for BLTA protein expression. Compared with NC, the miR-155 inhibitor decreased miR-155 by about 45%, but did not influence BTLA mRNA expression. Compared with NC, the miR-155 inhibitor decreased the surface BTLA expression by about 60%. Upregulation of BTLA in miR-155 knockdown CD4+ T cells did not influence the cell surface expression of CD69, an early activation marker (p=0.523). Similarly, IL-2 production was not changed. <br/><strong>Conclusion</strong>: miR-155 is involved in the inhibition of BTLA during CD4+ T cell activation. These results might serve as a basis for an eventual therapeutic manipulation of this pathway to treat inflammatory and autoimmune diseases.en_US
dc.languageEnglish
dc.language.isoen_US
dc.publisherShiraz Institute for Cancer Researchen_US
dc.relation.ispartofIranian Journal of Immunologyen_US
dc.subjectActivationen_US
dc.subjectB and T Lymphocyte Attenuatoren_US
dc.subjectmiR-155en_US
dc.subjectNaïve CD4+ T Cellen_US
dc.titleB and T Lymphocyte Attenuator is a Target of miR-155 during Naive CD4+ T Cell Activationen_US
dc.typeTexten_US
dc.typeOriginal Articleen_US
dc.contributor.departmentDepartment of Intensive Care Medicine, Hospital of PLAen_US
dc.contributor.departmentDepartment of Respiratory Disease, Shanghai Changzheng Hospital, Second Military Medical Universityen_US
dc.contributor.departmentDepartment of Respiratory Disease, Shanghai Changzheng Hospital, Second Military Medical Universityen_US
dc.contributor.departmentDepartment of Respiratory Medicine, Hospital of PLAen_US
dc.contributor.departmentDepartment of Medical Oncology, Shanghai Changzheng Hospital, Second Military Medical, University, Shanghai, Chinaen_US
dc.contributor.departmentDepartment of Respiratory Disease, Shanghai Changzheng Hospital, Second Military Medical Universityen_US
dc.citation.volume13
dc.citation.issue2
dc.citation.spage89
dc.citation.epage99


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