T-independent activation of B cells by vesicular stomatitis virus: No evidence for the need of a second signal

T-independent activation of B cells by vesicular stomatitis virus: No evidence for the need of a second signal
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DOI:
10.1006/cimm.1996.0065
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发表时间:
1996-03-15
影响因子:
4.3
通讯作者:
Zinkernagel, RM
Zinkernagel, RM
中科院分区:
医学4区
文献类型:
--
作者:
Fehr, T;Bachmann, MF;Zinkernagel, RM

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水泡性口炎病毒(VSV)诱导不依赖于T辅助细胞的IgM抗体应答,而IgG应答是严格依赖于T辅助细胞的。由于VSV在完全不存在T辅助细胞的情况下诱导B细胞,因此出现了这样的问题,即这种诱导是否在不存在第二信号的情况下发生,或者它是否依赖于替代或替换信号2,因此,我们询问VSV是否具有多克隆B细胞刺激活性和/或VSV诱导的B细胞是否需要通过补体或肿瘤坏死因子(TNF)受体或通过自然杀伤(NK)细胞活性的共刺激,体外B细胞增殖测定和CD 40缺陷小鼠体内抗体应答分析排除了VSV具有多克隆B细胞刺激物的性质,眼镜蛇毒因子对C3的消耗和抗补体受体抗体的应用表明,除了在非常有限的抗原剂量下,T-非依赖性IgM应答在很大程度上是C3-非依赖性的,TNF受体缺陷小鼠的免疫显示出正常的抗VSV IgM应答,并且在对YAC靶细胞的细胞毒性测定中,没有VSV激活NK细胞的证据。因此,VSV似乎诱导B细胞而没有多克隆激活和/或C3、TNF或NK细胞作为替代第二信号。(C)出版社:Academic Press,Inc.
Vesicular stomatitis virus (VSV) induces a T helper cell-independent IgM antibody response, whereas the IgG response is strictly T helper cell dependent, Since VSV induces B cells in complete absence of T helper cells, the question arises as to whether this induction occurs in the absence of a second signal or whether it depends upon an alternative or replacing signal 2, We therefore asked whether VSV has polyclonal B cell stimulator activity and/or whether B cell induction by VSV needs costimulation via complement or tumor necrosis factor (TNF) receptor or by natural killer (NK) cell activity, In vitro B cell proliferation assays and analysis of the in vivo antibody response in CD40 deficient mice excluded that VSV has properties of a polyclonal B cell stimulator, C3 depletion by cobra venom factor and application of anti-complement receptor antibodies showed that the T-independent IgM response was largely C3-independent except under very limiting antigen doses, Immunization of TNF receptor-deficient mice showed a normal anti-VSV IgM response, and in a cytotoxicity assay on YAC target cells there was no evidence for NK cell activation by VSV, Thus, VSV seems to induce B cells without polyclonal activation and/or C3, TNF, or NK cells functioning as a replacing second signal. (C) 1996 Academic Press, Inc.