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Role of the major histocompatibility complex in T cell activation of B cell subpopulations. A single monoclonal T helper cell population activates different B cell subpopulations by distinct pathways

机译:主要组织相容性复合物在B细胞亚群的T细胞活化中的作用。单个单克隆T辅助细胞群体通过不同途径激活不同的B细胞亚群

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摘要

It has recently been demonstrated that the Lyb-5+ and Lyb-5- B cell subpopulations differ in their requirements for major histocompatibility complex (MHC)-restricted activation by T helper (TH) cells. To determine whether these MHC-restricted and -unrestricted pathways of B cell activation result from differences in the participating TH cell populations or reflect differences exclusively in the responding B cell subpopulations, experiments were carried out using cloned TH cells for in vitro antibody responses to trinitrophenyl- keyhole limpet hemocyanin. The same cloned T helper cells were able to activate both CBA/N (Lyb-5-) B cells and CBA/CaHN (Lyb-5+ + Lyb-5-) B cells under different experimental conditions. The activation of Lyb-5- B cells by cloned T helper cells required both MHC-restricted TH cell-B cell interaction and carrier-hapten linkage. In contrast, the activation of Lyb-5+ B cells required only MHC-restricted T helper cell interaction with accessory cells, while T-B interaction was MHC unrestricted and did not require carrier-hapten linkage. Thus, the differences in activation requirements observed for the Lyb-5- and Lyb- 5+ B cell subsets do not result from differences in the TH cell populations activating these B cells, but rather reflect differences in the ability of these B cells to respond to signals from the same TH cells.
机译:最近已经证明,Lyb-5 +和Lyb-5-B细胞亚群在主要组织相容性复合物(MHC)限制的T辅助(TH)细胞激活方面的要求不同。为了确定这些MHC限制和非限制的B细胞活化途径是由​​参与的TH细胞群体的差异引起还是仅反映了应答B细胞亚群的差异,使用克隆的TH细胞进行了针对三硝基苯基的体外抗体反应的实验-匙孔血蓝蛋白。在不同的实验条件下,相同的克隆的T辅助细胞能够激活CBA / N(Lyb-5-)B细胞和CBA / CaHN(Lyb-5 + + Lyb-5-)B细胞。克隆的T辅助细胞对Lyb-5-B细胞的激活需要MHC限制的TH细胞-B细胞相互作用和载体-半抗原连接。相反,Lyb-5 + B细胞的激活仅需要MHC限制的T辅助细胞与辅助细胞相互作用,而T-B相互作用不受MHC限制并且不需要携带者-半抗原连接。因此,对于Lyb-5-和Lyb-5 + B细胞亚群观察到的激活要求的差异不是由激活这些B细胞的TH细胞群体的差异引起的,而是反映了这些B细胞响应能力的差异来自相同TH细胞的信号

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