The staphylococcal toxic shock syndrome toxin 1 triggers B cell proliferation and differentiation via major histocompatibility complex-unrestricted cognate T/B cell interaction.
The staphylococcal toxic shock syndrome toxin 1 triggers B cell proliferation and differentiation via major histocompatibility complex-unrestricted cognate T/B cell interaction.
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DOI：
10.1084/jem.170.6.2011
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发表时间：
1989-12-01
期刊：
影响因子：
--
通讯作者：
Chatila T
中科院分区：
文献类型：
--
作者：
Mourad W;Scholl P;Diaz A;Geha R;Chatila T
金黄色葡萄球菌外毒素中毒性休克综合征毒素1(TSST-1)是一种有效的T细胞和单核细胞激活剂。我们最近证明了TSST-1是一种超抗原，可以与MHC II类分子上的单态决定簇结合。在本研究中，我们检测了TSST-1对高密度人扁桃体B细胞活化和分化的影响。TSST-1以高亲和力和饱和动力学与扁桃体B细胞结合。这种结合可被抗人类白细胞抗原DR和抗人类白细胞抗原DQ单抗联合有效地抑制。用TSST-1处理纯化的B细胞不能诱导B细胞增殖或产生Ig。然而，在照射的T细胞存在的情况下，TSST-1诱导静息B细胞增殖并分化为Ig分泌细胞。TSST-1类似于名义抗原，其诱导B细胞反应严格依赖于T和B细胞之间的物理接触，并被抗MHC II类单抗、抗CD3单抗和较小程度的抗CD18单抗所抑制。然而，与名义抗原不同的是，TSST-1介导的T/B细胞相互作用是不受MHC限制的。这些结果表明，TSST-1通过TCR/CD3复合体和MHCⅡ类抗原介导MHC与同源T/B细胞的非限制性相互作用，从而诱导T细胞依赖的B细胞的增殖和分化。
The Staphylococcus aureus exotoxin toxic shock syndrome toxin 1 (TSST- 1) is a potent activator of T cells and monocytes. We have recently demonstrated that TSST-1 is a superantigen that binds monomorphic determinants on MHC class II molecules. In the present study, we have examined the effect of TSST-1 on the activation and differentiation of high density human tonsillar B cells. TSST-1 bound to tonsilar B cells with high affinity and saturation kinetics. This binding was effectively inhibited by a combination of anti-HLA-DR and anti-HLA-DQ mAbs. Treatment of purified B cells with TSST-1 failed to induce B cell proliferation or Ig production. However, in the presence of irradiated T cells, TSST-1 induced resting B cells to proliferate and differentiate into Ig secretory cells. TSST-1 mimicked nominal antigen in that its induction of B cell responses was strictly dependent on physical contact between T and B cells, and was profoundly inhibited by anti-MHC class II mAbs, anti-CD3 mAbs, and, to a lesser extent, by anti- CD18 mAbs. However, unlike nominal antigen, TSST-1-mediated T/B cell interactions were MHC unrestricted. These results suggest that TSST-1 induces T cell-dependent B cell proliferation and differentiation by virtue of its ability to mediate MHC-unrestricted cognate T/B cell interaction via the TCR/CD3 complex and MHC class II antigens.