title: Expression of T-cell receptor V beta 2 and type 1 helper T-cell-related cytokine mRNA in streptococcal pyrogenic exotoxin-C-activated human peripheral blood mononuclear cells.
abstract: Streptococcal pyrogenic exotoxin type C (SPE C) is a member of the bacterial superantigens that are potent stimulants of T cells. We expressed SPE C in Escherichia coli and characterized its selective stimulation properties on human T cells bearing specific V beta chains of T-cell receptors (TCRs). Cytokine profiles induced by SPE C were also examined. Recombinant SPE C significantly enhanced proliferation of human peripheral blood mononuclear cells (PBMCs) at concentrations as low as 10(-12)-10(-14)M. Reverse transcription of RNA, from SPE-C-stimulated PBMCs followed by polymerase chain reaction, revealed selective induction of TCR V beta 2 chain expression. SPE C raised the mRNA level of type 1 helper T cell (TH1) related cytokines, such as interferon gamma (IFN-gamma), interleukin 2 (IL-2), and tumor necrosis factor beta (TNF beta). The expression of TNF alpha was also increased. In contrast, the increase in mRNA levels of the p35 small fragment of IL-12 and type 2 helper T cell (TH2) related cytokines (i.e., IL-4 and IL-10) was not significantly affected by SPE C. The mRNA level of proinflammatory cytokine IL-6 was increased marginally. Consistent with the mRNA accumulation, protein concentrations of IFN gamma, IL-2, and TNF were increased in SPE-C-stimulated PBMCs, but IL-4 was not. From these results, we conclude that the stimuli of SPE C preferentially causes the TH1 responses in human T cells bearing TCR V beta 2.
authors.affiliation: Department of Microbiology, School of Dentistry, Iwate Medical University, Morioka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ohara-Nemoto
authors.forename: M
authors.initials: M
authors.lastname: Kaneko
mesh_terms: D001426:Bacterial Proteins; D003001:Cloning, Molecular; D004926:Escherichia coli / Q000235:genetics; D005098:Exotoxins / Q000235:genetics* / Q000276:immunology*; D015964:Gene Expression Regulation, Bacterial; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis / Q000096:biosynthesis; D007378:Interleukins / Q000032:analysis / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000382:microbiology*; D008233:Lymphotoxin-alpha / Q000032:analysis / Q000096:biosynthesis; D008565:Membrane Proteins; D010957:Plasmids; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000096:biosynthesis*; D013297:Streptococcus pyogenes / Q000235:genetics*; D018089:Superantigens / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000096:biosynthesis
chemical_list: D001426:Bacterial Proteins; D005098:Exotoxins; D007378:Interleukins; D008233:Lymphotoxin-alpha; D008565:Membrane Proteins; D012333:RNA, Messenger; D016693:Receptors, Antigen, T-Cell, alpha-beta; C117980:SpeA protein, Streptococcus pyogenes; D018089:Superantigens; D014409:Tumor Necrosis Factor-alpha; C027951:erythrogenic toxin; D007371:Interferon-gamma