Interaction of toxin-1 and T lymphocytes in toxic shock syndrome.

Toxic shock syndrome (TSS) is a potentially fatal illness caused by infection with the bacterium Staphylococcus aureus. TSS toxin-1 (TSST-1) contains a T-cell epitope with specificity for human V-beta-2. Binding of TSST-1 to the human major histocompatibility complex and T cell receptors activates T cells and triggers the secretion of high amounts of inflammatory cytokines, leading to TSS and potentially death. During this process, CD4+ T cells are inhibited by TSST-1, while regulatory T cells are increased. This suggests a protective immune response by the body in TSS. Thus, TSST-1 can trigger both, an inflammatory response that attacks the body and a protective response. In this review, we discuss the interaction between TSST-1 and T lymphocytes in TSS.

[Construction and identification of adenovirus vector for double-mutant human hypoxia-inducible factor-1alpha gene].

OBJECTIVE: To construct an adenovirus vector containing the double-mutant hypoxia-inducible factor-1alpha (HIF-1alpha) gene for exploring the therapeutic angiogenesis for coronary heart disease. METHODS: Human double-mutant HIF-1alpha cDNA was obtained from PCR of pShuttle-2-HIF-1alpha containing the mutant HIF-1alpha gene (564). The recombinant adenoviral plasmid containing mutant HIF-1alpha cDNA was constructed by ligation of recombinant pShuttle2 containing double-mutant HIF-1alpha cDNA and Adeno-X viral DNA, followed by its identification and transfection into adenoviral packaging cells HEK293 via lipofectamine 2000. RESULT AND CONCLUSION: The recombinant pAdeno-HIF-1alpha was correctly constructed and verified by restriction endonuclease and DNA sequencing analyseis. This recombinant adenovirus containing the double-mutant HIF-1alpha gene may facilitate further investigation of mutant HIF-1alphagene therapy for coronary heart disease.