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Lack of galectin-3 up-regulates IgA expression by peritoneal B1 lymphocytes during B cell differentiation
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  • 作者:Felipe L. Oliveira ; Emerson S. Bernardes ; Camila Brand…
  • 关键词:Peritoneal cavity ; B lymphocytes ; Plasma cells ; IgA ; Galectin ; 3 ; Mast cells ; Mouse ; Schistosoma mansoni
  • 刊名:Cell and Tissue Research
  • 出版年:2016
  • 出版时间:February 2016
  • 年:2016
  • 卷:363
  • 期:2
  • 页码:411-426
  • 全文大小:16,285 KB
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  • 作者单位:Felipe L. Oliveira (1)
    Emerson S. Bernardes (2)
    Camila Brand (1)
    Sofia N. dos Santos (2)
    Mariana P. Cabanel (1)
    Kátia D. Arcanjo (1)
    José M. Brito (1)
    Radovan Borojevic (1)
    Roger Chammas (3) (4)
    Márcia C. El-Cheikh (1)

    1. Laboratório de Proliferação e Diferenciação Celular – Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Avenida Carlos Chagas Filho, 373 – CCS – Bloco F – 2° andar – Sala 1, 21941-902, Rio de Janeiro, Brazil
    2. Radiopharmacy Center, Institute of Energy and Nuclear Research (IPEN), São Paulo, SP, Brazil
    3. Laboratório de Oncologia Experimental, Departamento de Radiologia e Oncologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil
    4. Instituto do Câncer do Estado de São Paulo, São Paulo, SP, Brazil
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Biomedicine
    Human Genetics
    Proteomics
    Molecular Medicine
  • 出版者:Springer Berlin / Heidelberg
  • ISSN:1432-0878
文摘
Galectin-3 is a β-galactoside-binding protein with an inhibitory role in B cell differentiation into plasma cells in distinct lymphoid tissues. We use a model of chronic schistosomiasis, a well-characterized experimental disease hallmarked by polyclonal B cell activation, in order to investigate the role of galectin-3 in controlling IgA production through peritoneal B1 cells. Chronically infected, galectin-3-deficient mice (Lgals3 −/−) display peritoneal fluid hypercellularity, increased numbers of atypical peritoneal IgM+/IgA+ B1a and B1b lymphocytes and histological disturbances in plasma cell niches when compared with Lgals3 +/+ mice. Similar to our infection model, peritoneal B1 cells from uninfected Lgals3 −/− mice show enhanced switching to IgA after in vitro treatment with interleukin-5 plus transforming growth factor-β (IL-5 + TGF-β1). A higher number of IgA+ B1a lymphocytes was found in the peritoneal cavity of Lgals3 −/−-uninfected mice at 1 week after i.p. injection of IL-5 + TGF-β1; this correlates with the increased levels of secreted IgA detected in the peritoneal fluid of these mice after cytokine treatment. Interestingly, a higher number of degranulated mast cells is present in the peritoneal cavity of uninfected and Schistosoma mansoni-infected Lgals3 −/− mice, indicating that, at least in part, mast cells account for the enhanced differentiation of B1 into IgA-producing B cells found in the absence of galectin-3. Thus, a novel role is revealed for galectin-3 in controlling the expression of surface IgA by peritoneal B1 lymphocytes; this might have important implications for manipulating the mucosal immune response. Keywords Peritoneal cavity B lymphocytes Plasma cells IgA Galectin-3 Mast cells Mouse Schistosoma mansoni

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