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Splenic macrophages maintain the anti‐platelet autoimmune response via uptake of opsonized platelets in patients with immune thrombocytopenic purpura

KUWANA, M. ; OKAZAKI, Y. ; IKEDA, Y.

Journal of thrombosis and haemostasis, 2009-02, Vol.7 (2), p.322-329 [Periódico revisado por pares]

Oxford, UK: Blackwell Publishing Ltd

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  • Título:
    Splenic macrophages maintain the anti‐platelet autoimmune response via uptake of opsonized platelets in patients with immune thrombocytopenic purpura
  • Autor: KUWANA, M. ; OKAZAKI, Y. ; IKEDA, Y.
  • Assuntos: Antigen Presentation - immunology ; Antigen-Presenting Cells - immunology ; antigen‐presenting cell ; anti‐platelet antibody ; Autoimmunity - immunology ; B-Lymphocytes ; Blood Platelets - immunology ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells ; Humans ; immune thrombocytopenic purpura ; macrophage ; Macrophages - immunology ; Opsonin Proteins - metabolism ; Platelet Glycoprotein GPIIb-IIIa Complex - immunology ; Purpura, Thrombocytopenic, Idiopathic - immunology ; Receptors, IgG - immunology ; Spleen ; T cell ; T-Lymphocytes
  • É parte de: Journal of thrombosis and haemostasis, 2009-02, Vol.7 (2), p.322-329
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Background: Immune thrombocytopenic purpura (ITP) is an autoimmune disease primarily caused by IgG anti‐platelet autoantibodies. Activation of autoreactive CD4+ T cells upon recognition of cryptic GPIIb/IIIa peptides presented by antigen‐presenting cells (APCs) is a critical step for triggering and maintaining the pathogenic anti‐platelet autoantibody response. Objectives: We investigated which APCs carry the cryptic peptides of GPIIb/IIIa that activate autoreactive CD4+ T cells in ITP patients. Methods: GPIIb/IIIa‐reactive T‐cell lines generated from ITP patients were cultured with autologous freshly isolated splenic macrophages, B cells or dendritic cells. To further investigate how the macrophages presented the antigenic GPIIb/IIIa peptides, we prepared macrophages from the peripheral blood monocytes of the same patients during remission. Results: Macrophages induced the proliferation of GPIIb/IIIa‐reactive T‐cell lines without an exogenous antigen, but B cells and dendritic cells required GPIIb/IIIa peptides to stimulate the T cells. Macrophages derived from peripheral blood during remission required an exogenous antigen to induce the GPIIb/IIIa‐reactive T‐cell line response, but could elicit a response without added antigen if they were preincubated with platelets from ITP patients with platelet‐associated anti‐GPIIb/IIIa antibodies or healthy platelets pretreated with ITP platelet eluates. The T‐cell response was inhibited by anti‐FcγRI antibody. Finally, cultured macrophages that captured opsonized platelets promoted anti‐GPIIb/IIIa antibody production in mixed cultures of autologous GPIIb/IIIa‐reactive T‐cell lines and B cells. Conclusions: Splenic macrophages that take up opsonized platelets via FcγRI are major APCs for cryptic GPIIb/IIIa peptides, and are central to the maintenance of anti‐platelet autoantibody production in ITP patients.
  • Editor: Oxford, UK: Blackwell Publishing Ltd
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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