The role of CD83 in the pathogenesis of immune thrombocytopenia.

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  • Additional Information
    • Source:
      Publisher: Taylor & Francis Country of Publication: England NLM ID: 9708388 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1607-8454 (Electronic) Linking ISSN: 10245332 NLM ISO Abbreviation: Hematology Subsets: MEDLINE
    • Publication Information:
      Publication: 2016- : Abingdon : Taylor & Francis
      Original Publication: [Amsterdam] : Newark, NJ : Harwood Academic Publishers ; International Publishers Distributor,
    • Subject Terms:
    • Abstract:
      Background: CD83 are closely related to the pathogenesis of immune thrombocytopenia (ITP), but the exact mechanism remains unclear.
      Aim: To explore the relationship between CD83 and CD4 + T cell subsets and clarify the role of CD83 in the pathogenesis of ITP.
      Methods: RT-qPCR and Flow cytometry were used to illustrate CD83 expression. The downregulation and overexpression of DC-CD83 were co-cultured with CD4 + T cells to detect cell proliferation, co-cultured supernatant cytokines and Tregs expression.
      Results: The results indicate that the ITP patients showed higher expression of CD83 than the healthy controls. The proliferation of CD4 + T cells was inhibited by downregulation of DCs-CD83 but promoted by overexpression of DCs-CD83. siRNA-CD83 inhibited proinflammatory IFN-γ and IL-17 secretion while raising TGF-β, IL-10 concentrations. Overexpression of DCs-CD83 promoted Tregs expression.
      Conclusion: The Th1/Th2 and Th17/Tregs polarization were reversed via interfering DCs with siRNA-CD83. CD83 plays an important role in ITP pathogenesis, suggesting novel treatment for ITP patients.
    • Contributed Indexing:
      Keywords: CD4+ T cell; CD83; Immune thrombocytopenia; cytokines; dendritic cells; immune; overexpression; siRNA
    • Accession Number:
      0 (CD83 Antigen)
      0 (Membrane Glycoproteins)
      0 (Antigens, CD)
      0 (Immunoglobulins)
      0 (Cytokines)
    • Publication Date:
      Date Created: 20240712 Date Completed: 20240712 Latest Revision: 20240712
    • Publication Date:
      20240712
    • Accession Number:
      10.1080/16078454.2024.2372482
    • Accession Number:
      38994874