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首页> 外文期刊>The Journal of Experomental Medicine >Cross-linking of major histocompatibility complex class II molecules by staphylococcal enterotoxin A superantigen is a requirement for inflammatory cytokine gene expression.
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Cross-linking of major histocompatibility complex class II molecules by staphylococcal enterotoxin A superantigen is a requirement for inflammatory cytokine gene expression.

机译：主要组织相容性复合物II类分子通过葡萄球菌肠毒素A的超交联是炎症细胞因子基因表达的必要条件。

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摘要

Staphylococcal enterotoxin A (SEA) has two distinct binding sites for major histocompatibility complex (MHC) class II molecules. The aspartic acid located at position 227 (D227) in the COOH terminus of SEA is one of the three residues involved in its interaction with the DR beta chain, whereas the phenylalanine 47 (F47) of the NH2 terminus is critical for its binding to the DR alpha chain. Upon interaction with MHC class II molecules, SEA triggers several cellular events leading to cytokine gene expression. In the present study, we have demonstrated that, contrary to wild-type SEA, stimulation of the THP1 monocytic cell line with SEA mutated at position 47 (SEAF47A) or at position 227 (SEAD227A) failed to induce interleukin 1 beta and tumor necrosis factor-alpha messenger RNA expression. Pretreatment of the cells with a 10-fold excess of either SEAF47A or SEAD227A prevented the increase in cytokine messenger RNA induced by wild-type SEA. However, cross-linking of SEAF47A or SEAD227A bound to MHC class II molecules with F(ab')2 anti-SEA mAb leads to cytokine gene expression, whereas cross-linking with F(ab) fragments had no effect. Taken together, these results indicate that cross-linking of two MHC class II molecules by one single SEA molecule is a requirement for cytokine gene expression.
机译：葡萄球菌肠毒素A（SEA）具有两个主要组织相容性复合体（MHC）II类分子的不同结合位点。位于SEA的COOH末端227位（D227）的天冬氨酸是其与DRβ链相互作用所涉及的三个残基之一，而NH2末端的苯丙氨酸47（F47）对于与其结合至关重要。 DR alpha链。与II类MHC分子相互作用后，SEA会触发一些细胞事件，导致细胞因子基因表达。在本研究中，我们已经证明，与野生型SEA相反，用在47位（SEAF47A）或227位（SEAD227A）突变的SEA刺激THP1单核细胞系不能诱导白介素1β和肿瘤坏死因子-alpha信使RNA表达。用10倍过量的SEAF47A或SEAD227A预处理细胞可防止野生型SEA诱导的细胞因子信使RNA的增加。但是，与MHC II类分子结合的SEAF47A或SEAD227A与F（ab'）2抗SEA mAb的交联导致细胞因子基因表达，而与F（ab）片段的交联则没有作用。综上所述，这些结果表明两个MHC II类分子与一个SEA分子的交联是细胞因子基因表达的必要条件。

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