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中毒性休克综合征毒素-1对小鼠T细胞的激活作用。小鼠辅助细胞上表达的毒素结合结构是MHC II类分子。

Activation of murine T cells by toxic shock syndrome toxin-1. The toxin-binding structures expressed on murine accessory cells are MHC class II molecules.

作者信息

Uchiyama T, Tadakuma T, Imanishi K, Araake M, Saito S, Yan X J, Fujikawa H, Igarashi H, Yamaura N

机构信息

Department of Microbiology, Tokyo Women's Medical College, Japan.

出版信息

J Immunol. 1989 Nov 15;143(10):3175-82.

PMID:2509554
Abstract

Toxic shock syndrome toxin-1 (TSST-1)-binding structures present on murine lymphoid tissues were investigated by using 125I-TSST-1. T-depleted C57BL/6 spleen cells incubated with TSST-1 for 3 h at 0 degree C were mitogenic to splenic T cells, indicating that the former cells bind and present TSST-1 to T cells. TSST-1-binding activity was observed in C57BL/6 splenic B cells and L cells transfected with I-Ab genes, but not in splenic T cells and control L cells. Scatchard plot analysis showed that these B cells and transfectants bound TSST-1 with similar binding affinity. SDS-PAGE analysis showed that lysates of C57BL/6 spleen cells and the I-Ab-positive transfectants contain a single band which bound TSST-1 and comigrated with I-Ab heterodimers. TSST-1-binding activity observed clearly in C57BL/6. BALB/c, and C3H/HeN spleen cells and L cells transfected with I-Ab or I-Ak genes was not reduced by paraformaldehyde fixation. Binding of 125I-TSST-1 to the three spleen cells was markedly reduced by anti-I-A antibodies, but not by anti-I-E antibodies. C57BL/6, C3H/HeN, and (C3H/HeN x C57BL/6) F1 T cells were activated by TSST-1 to proliferate and produce IL-2 in the presence of FT6.2 cells, LT1-30-3 cells and either of them, respectively, but not in the presence of control L cells. These results indicate that I-A molecules function as the structures via that accessory cells directly bind TSST-1 on the cell surface and present a triggering signal of TSST-1 to T cells.

摘要

利用¹²⁵I-中毒性休克综合征毒素-1(TSST-1)研究了鼠类淋巴组织上存在的TSST-1结合结构。在0℃下与TSST-1孵育3小时的T细胞缺失的C57BL/6脾细胞对脾T细胞有丝分裂原性,表明前者细胞能结合TSST-1并将其呈递给T细胞。在转染了I-Ab基因的C57BL/6脾B细胞和L细胞中观察到TSST-1结合活性,但在脾T细胞和对照L细胞中未观察到。Scatchard作图分析表明,这些B细胞和转染子以相似的结合亲和力结合TSST-1。SDS-PAGE分析表明,C57BL/6脾细胞和I-Ab阳性转染子的裂解物含有一条与TSST-1结合并与I-Ab异二聚体共迁移的单带。在C57BL/6、BALB/c和C3H/HeN脾细胞以及转染了I-Ab或I-Ak基因的L细胞中清楚观察到的TSST-1结合活性,不会因多聚甲醛固定而降低。¹²⁵I-TSST-1与三种脾细胞的结合被抗I-A抗体显著降低,但不被抗I-E抗体降低。在分别存在FT6.2细胞、LT1-30-3细胞以及二者之一的情况下,C57BL/6、C3H/HeN和(C3H/HeN×C57BL/6)F1 T细胞被TSST-1激活而增殖并产生IL-2,但在存在对照L细胞的情况下则不然。这些结果表明,I-A分子作为辅助细胞通过其直接在细胞表面结合TSST-1并将TSST-1的触发信号呈递给T细胞的结构发挥作用。

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