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    Online Resource
    Online Resource
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 143.35-143.35
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 143.35-143.35
    Abstract: The effect of B cell depletion on diabetogenic T cells is not fully understood. We generated hCD20BDC2.5 NOD mice to specifically address this question. We treated hCD20BDC2.5 NOD mice with 2H7 or control IgG.Our results showed that dividing BDC2.5 cells from 2H7 treated mice produced more IFNg than their counterparts from IgG treated mice (P=0.0035). Interestingly, circulating IFNg in serum of IgG treated mice was higher than that in 2H7 treated mice (p=0.0029). To investigate effect of B cell depletion on diabetogenicity of BDC2.5 T cells, we transferred purified CD4+ BDC2.5 T cells, from either 2H7 or IgG treated mice, into NOD/SCID mice. The overall incidence of diabetes was much higher in NOD/SCID mice received BDC2.5 CD4+ cells from 2H7 treated donors than that from IgG treated donors. To investigate the direct effect of B cells on diabetogenic CD4+ T cells, we co-transferred BDC2.5 CD4+ T cells with purified B cells from NOD mice. Interestingly, we found that B cells may have a protective effect as diabetes development was delayed in the NOD/SCID mice received more B cells. In vitro, the addition of B cells inhibited the proliferation of BDC2.5 CD4+ T cells, supporting the in vivo diabetes development results. In summary, B cell depletion affects pathogenic T cells and there is a dichotomy in the role of B cells in diabetes development.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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