ライフサイエンスコーパス: TSST-1

1 TSST-1 (100 microg/ml) caused up- or down-regulation of

2 TSST-1 also caused up-regulation of chemokine/cytokine g

3 TSST-1 induced shock via all three routes in rabbits.

4 TSST-1 not only represses most exoprotein genes but dete

5 TSST-1 was produced in medium alone in the absence of a

6 TSST-1, albeit less stable than SEC1 and SPEA to pepsin,

7 igens, most commonly toxic shock syndrome-1 (TSST-1), to specific TCR Vbeta-bearing T cells.

8 s and of positive antibodies to TSS toxin 1 (TSST-1) among 209 healthy Japanese women in Tokyo.

9 lococcal toxic shock syndrome (TSS) toxin 1 (TSST-1) and the streptococcal pyrogenic exotoxin A as lo

10 production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus aureus in vitro.

11 production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus aureus MN8 exposed to a range

12 expression of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus aureus was investigated under

13 Toxic shock syndrome toxin 1 (TSST-1) contains a long central alpha helix that forms t

14 tissue infections, whereas only TSS toxin 1 (TSST-1) is associated with menstrual, vaginal TSS.

15 ic function of toxic shock syndrome toxin 1 (TSST-1) is generally regarded as an important determinan

16 fects of toxic shock syndrome (TSS) toxin 1 (TSST-1) on the adaptive immune system, little is known a

17 xin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) resulted in enhanced production of gamma interfe

18 e superantigen toxic shock syndrome toxin 1 (TSST-1) results in the specific systemic expansion of hu

19 at presenting toxic shock syndrome toxin 1 (TSST-1) to T cells, suggesting that I-A(b)-associated pe

20 ) specific for toxic shock syndrome toxin 1 (TSST-1), a bacterial superantigen, showed the ability ei

21 production of toxic shock syndrome toxin 1 (TSST-1), enterotoxin, and other superantigens by coagula

22 igens, such as toxic shock syndrome toxin 1 (TSST-1), have been implicated in the pathogenesis of sev

23 protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly under low-oxygen conditions.

24 toxins SEB and toxic shock syndrome toxin 1 (TSST-1), the gene for SEl-K is commonly present in more

25 onization with toxic shock syndrome toxin 1 (TSST-1)-producing Staphylococcus aureus in women with in

26 h KD, secretes toxic shock syndrome toxin 1 (TSST-1).

27 xin B (SEB) or toxic shock syndrome toxin 1 (TSST-1).

28 Responses to toxic shock syndrome toxin-1 (TSST-1) and pokeweed mitogen (PWM) were inhibited at hig

29 superantigens toxic shock syndrome toxin-1 (TSST-1) and staphylococcus enterotoxin B (SEB) induced g

30 bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, we performed alanine scanning mutag

31 ive mutants of toxic shock syndrome toxin-1 (TSST-1) have been determined.

32 l superantigen toxic shock syndrome toxin-1 (TSST-1) is a causative agent of this disease, but its st

33 he staphylococcal toxin toxic shock toxin-1 (TSST-1), a prototypic superantigen, induces in vitro tot

34 enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and streptococcal pyrogenic exotoxins] and anth

35 SAgs), such as toxic shock syndrome toxin-1 (TSST-1), are the main cause of toxic shock syndrome (TSS

36 o an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by toxigenic strains of Staphylococc

37 , the gene for toxic shock syndrome toxin-1 (TSST-1), is part of a 15.2 kb genetic element in Staphyl

38 plied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal enterotoxin type B, and streptoc

39 fects of superantigens, such as TSS toxin-1 (TSST-1), than are mice.

40 gent of TSS is toxic shock syndrome toxin-1 (TSST-1), which is unique relative to other bacterial SAG

41 6 strains were the same toxic shock toxin-1 (TSST-1)-positive clone, designated electrophoretic type

42 n C (SEC), and toxic shock syndrome toxin-1 (TSST-1).

43 high levels of toxic shock syndrome toxin-1 (TSST-1).

44 A [SEA], SEB, toxic shock syndrome toxin 1 [TSST-1]) which act both as superantigens (SAgs) and toxi

45 construct a docking model for the hVbeta2.1-TSST-1 complex.

46 Of the 12 TSST-1-positive strains isolated, 6 (50%) were pulsed-fi

47 ne vaginal tissue, increased the flux of 35S-TSST-1 across the mucosal surface.

48 Receptor binding studies showed that 35S-TSST-1 bound to 5 x 10(4) receptors per HVEC, with satur

49 elve of 209 women (6%) were colonized with a TSST-1-producing strain; two (<1%) had vaginal colonizat

50 In addition, TSST-1 induced on B cells the expression of B7.2, a mole

51 While all mice co-administered TSST-1 and control Ig died, 75% of the CTLA4Ig plus TSST

52 Cs given after TSST-1 also did not inhibit enhancement of LPS-induced s

53 90% in vitro, it also strikingly ameliorated TSST-1 induced TSS in vivo.

54 ted production of agr RNAIII, protein A, and TSST-1, particularly under low-oxygen conditions.

55 nteractions of TSS Staphylococcus aureus and TSST-1 with human vaginal epithelial cells (HVECs) and p

56 responding proteins induced by S. aureus and TSST-1.

57 gned to determine S. aureus colonization and TSST-1 serum antibody titers in 3,012 menstruating women

58 pendent, facilitated transcytosis of SEB and TSST-1, but not SEA.

59 our strategy works equally well for SEB and TSST-1, two widely different phylogenic variants, sugges

60 against three different SAgs, SEB, SEC3, and TSST-1.

61 e staphylococcal enterotoxins, SEA, SEE, and TSST-1.

62 portant in promoting the development of anti-TSST-1 antibodies, as there was a significant difference

63 BL/6 mice with anti-MIF antibody 2 hr before TSST-1 injection prevented spleen enlargement and reduce

64 CTLA4Ig not only blocked TSST-1-stimulated T cell proliferation by 90% in vitro,

65 A MAb capable of detecting DR-bound TSST-1 could also inhibit the toxin-induced activation o

66 serum levels of TNF-alpha and IFN-gamma, but TSST-1-triggered IL-2 release was not affected.

67 nhancement of LPS-induced serum TNF-alpha by TSST-1 but inhibited the enhancement effect of TSST-1 on

68 pheral blood mononuclear cells stimulated by TSST-1 during the pollen season.

69 Most colonizing TSST-1-producing S. aureus strains in Japan were genotyp

70 In contrast, TSST-1-induced IFN-gamma was not significantly reduced i

71 In thin-film cultures, TSST-1 production increased from nearly undetectable lev

72 antigen, showed the ability either to detect TSST-1 bound to histocompatibility locus antigen (HLA)-D

73 g effect correlated with markedly diminished TSST-1 induced serum levels of TNF-alpha and IFN-gamma,

74 In the absence of carbon dioxide, TSST-1 production in batch cultures increased from negli

75 with class II MHC-positive HUVECs and either TSST-1 or SEB resulted in V(beta)-restricted CD69 up-reg

76 xin B 121-136, onto T2-I-A(b) cells enhanced TSST-1 presentation >1000-fold.

77 r their endotoxins (LTA + PGN) or exotoxins (TSST-1).

78 in vaginal mucosa permeability, facilitating TSST-1 penetration.

79 y CD4 and CD8 cells (V(beta)2 activation for TSST-1; V(beta)3, V(beta)5.1, and V(beta)12 activation f

80 erate a panel of high affinity receptors for TSST-1.

81 us to generate a map of the binding site for TSST-1 and to construct a docking model for the hVbeta2.

82 through a culture growing at a t(d) of 9 h, TSST-1 production increased significantly (by 3.4-fold)

83 nited States (89% and 75%, respectively) had TSST-1 antibodies.

84 erved SAG residues (Leu(137) and Tyr(144) in TSST-1).

85 t in Staphylococcus aureus that is absent in TSST-1-negative strains.

86 ions of APC are equally peptide dependent in TSST-1 presentation.

87 ) resulted in a 5.1- to 6.8-fold increase in TSST-1 production over that during anaerobic growth and

88 )-remainder N(2) was studied, no increase in TSST-1 production was observed; this was also the case w

89 equirement for CD28 costimulatory signals in TSST-1-induced TSS.

90 cus antigen (HLA)-DR molecules or to inhibit TSST-1 binding to HLA-DR.

91 tigenicity in a BALB/c mouse model of lethal TSST-1-induced hypersensitivity to lipopolysaccharide (L

92 tation of staphylococcal enterotoxin A, like TSST-1, is peptide dependent, whereas staphylococcal ent

93 Based on these data, a model of the MHC/TSST-1/TCR ternary complex predicts similarities seen wi

94 In this model, TSST-1 greatly potentiated both LPS-induced lethality, a

95 Moreover, TSST-1 stimulation of peripheral blood mononuclear cells

96 However, a mutant TSST-1 protein that fails to bind HLA-DR did not elicit

97 that this rear loop mediates the ability of TSST-1 to induce lethality and suggests a route for prod

98 g potent modulators of the toxic activity of TSST-1.

99 esults may explain the unique association of TSST-1 with menstrual TSS and why SPEA is only rarely as

100 ues exposed along this groove on the back of TSST-1.

101 critical insight into the molecular basis of TSST-1 specificity and serve as potential leads toward t

102 o completely inhibited the known capacity of TSST-1 to amplify LPS-induced levels of IFN-gamma in ser

103 oduction showed that lower concentrations of TSST-1 (10 pg/ml) were needed to release MIF than to ind

104 findings suggest that high concentrations of TSST-1 can induce IFN-gamma-dependent B cell apoptosis,

105 d B cell death occurred at concentrations of TSST-1 inducing the production of high amounts of gamma

106 ST-1 but inhibited the enhancement effect of TSST-1 on LPS-induced serum IFN-gamma by 50%.

107 ese agents reduced the enhancement effect of TSST-1 on LPS-induced serum TNF-alpha by 99 and 85%, res

108 ely susceptible to the enhancement effect of TSST-1 on LPS-induced serum TNF-alpha.

109 s report, we studied the in vitro effects of TSST-1 on B cell activation.

110 esistant to these LPS enhancement effects of TSST-1, BALB/c-SCID mice reconstituted with T cells were

111 The hierarchy of TSST-1 resistance among CD28 wild-type (CD28+/+), CD28 h

112 , mice given Cs after a priming injection of TSST-1, but before LPS, still exhibited lethal hypersens

113 l is proposed describing the interactions of TSST-1, ADAMs, and the EGFR that lead to establishment o

114 TSS isolates expressed comparable levels of TSST-1, consistent with previous findings.

115 B cells after stimulation with 1000 pg/ml of TSST-1 and was significantly higher on B cells undergoin

116 optosis after stimulation with 1000 pg/ml of TSST-1 compared with 1 or 0.01 pg/ml of toxin or medium

117 In a lethal mouse model of TSST-1-induced shock, anti-MIF antibody increased surviv

118 helix and are useful in mapping portions of TSST-1 involved in superantigenicity and lethality.

119 s some peptides promoted the presentation of TSST-1 (almost 5,000-fold in the case of one peptide), o

120 plays a critical role in the presentation of TSST-1 by splenic APC and showed that different subpopul

121 ecule of the agr locus) and on production of TSST-1 (an exotoxin) and protein A (a surface-associated

122 her cotton nor rayon amplifies production of TSST-1 in vitro, and cotton tampons cannot be claimed to

123 yon differ in their effects on production of TSST-1 in vitro, two methods of bacterial cultivation, w

124 e and polyester foam increased production of TSST-1 to a large degree in both culture systems.

125 of srrB resulted in decreased production of TSST-1 under microaerobic conditions and, to a lesser ex

126 le and experimental tampons on production of TSST-1.

127 m, O(2) alone does not trigger production of TSST-1; rather, both CO(2) and O(2) are required.

128 teins that are extremely strong promoters of TSST-1 presentation (47,500- and 12,000-fold, respective

129 is within the putative TCR binding region of TSST-1 along the central alpha helix adjacent to the N-t

130 AB resulted in nearly complete repression of TSST-1 production in both microaerobic and aerobic condi

131 sidue likely accounts for the restriction of TSST-1 specificity to only this human Vbeta region.

132 g) inhibited rabbit lethality as a result of TSST-1 administered vaginally.

133 ctural basis for the high TCR specificity of TSST-1 and present a model of the TSST-1-dependent MHC-S

134 contributing to the TCR Vbeta specificity of TSST-1.

135 obility may be responsible for the spread of TSST-1 production among S. aureus strains.

136 Here, we report the crystal structure of TSST-1 in complex with an affinity-matured variant of it

137 ffect of neutralizing anti-MIF antibodies on TSST-1-induced lymphocyte proliferation and lethal toxic

138 effects of both oxygen and carbon dioxide on TSST-1 production.

139 In addition, the peptide effect on TSST-1 presentation has been demonstrated only in the co

140 differences between them in their effects on TSST-1.

141 n known to block costimulatory signaling, on TSST-1-induced responses.

142 s T-cell receptor Vbeta interaction sites on TSST-1 as determined by reactivity with a panel of recom

143 ect against challenge with a different SE or TSST-1, mice were vaccinated with SEA, SEB, SEC1, or TSS

144 while stimulation of these cells with SEB or TSST-1 resulted in suppressed IL-6 and TNF-alpha product

145 mice were vaccinated with SEA, SEB, SEC1, or TSST-1 individually or in combination.

146 /6 mice using CD8+ T cells from CTLA4Ig plus TSST-1-primed mice.

147 and control Ig died, 75% of the CTLA4Ig plus TSST-1-treated mice survived.

148 or the HLA-DR association site could present TSST-1 in vitro, stimulating CD4+ human T cells to proli

149 re we show that peptides that do not promote TSST-1 presentation can be converted into "promoting" pe

150 e been identified that significantly promote TSST-1 presentation.

151 ed by reactivity with a panel of recombinant TSST-1 mutant molecules.

152 ession of SrrAB, which represses agr RNAIII, TSST-1, and protein A in vitro, decreases virulence in t

153 Outside the pollen season, TSST-1 significantly increased total IgE production only

154 , they were completely resistant to a second TSST-1 challenge.

155 says of the agr P2, agr P3, protein A (spa), TSST-1 (tst), and srr promoters revealed SrrA binding at

156 resulted in a 7.6-fold increase in specific TSST-1 production.

157 train tested produced 6.1-fold more specific TSST-1 in a growth environment of 4% O(2)-10% CO(2)-86%

158 g time (t(d))-of 3 h, production of specific TSST-1 (expressed as micrograms per milligram of cell dr

159 To stimulate TSST-1 production, air and anaerobic gas were premixed b

160 analyzed this disparity and have found that TSST-1 itself is a negative global regulator of exoprote

161 We show herein that TSST-1 produced antagonistic effects on Ig synthesis by

162 model of the wild-type complex, we show that TSST-1 engages TCR ligands in a markedly different way t

163 These experiments support the theory that TSST-1-induced hypersensitivity to LPS is mediated prima

164 ificity of TSST-1 and present a model of the TSST-1-dependent MHC-SAG-TCR T-cell signaling complex th

165 ate the superantigen functional sites on the TSST-1 molecule and constitute reagents with the propert

166 Furthermore, this TSST-1 resistance could be transferred to naive C57BL/6

167 ound to have antibody titers (> or =1:32) to TSST-1 (89% versus 98% and 100%).

168 enagers have antibody titers (> or =1:32) to TSST-1 and are presumed to be protected from mTSS.

169 subjects had antibody titers (> or =1:32) to TSST-1, and the vast majority (81%) of teenaged subjects

170 and to develop high affinity antagonists to TSST-1, we used directed evolution to generate a panel o

171 stability and for higher affinity binding to TSST-1.

172 of the differential response by human DCs to TSST-1.

173 t the delayed and transferable resistance to TSST-1 was due, at least in part, to CD8+ T cells with s

174 t mice (CD28-/-) are completely resistant to TSST-1-induced lethal TSS while CD28 (+/-) littermate mi

175 littermate mice were partially resistant to TSST-1.

176 sal sites were characterized with respect to TSST-1 production and resistance genotype.

177 at the transcriptional level in response to TSST-1 and is also necessary for AREG, TGFalpha, and TNF

178 irment of IFN-gamma secretion in response to TSST-1 injection.

179 f genes up-regulated by HVECs in response to TSST-1 that includes the sheddase, a disintegrin and met

180 In response to TSST-1, human vaginal epithelial cells (HVECs) produce c

181 and IL-8 production by HVECs in response to TSST-1.

182 (TNFR1), are shed from HVECs in response to TSST-1.

183 United States, despite low seropositivity to TSST-1 in Japan.

184 e rabbits remained completely susceptible to TSST-1, indicating that TSS can occur in the setting of

185 s (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as superantigens to cause overstimulation of

186 the gene for the toxic shock syndrome toxin (TSST-1) and can be mobilized by infection with S. aureus

187 he production of toxic shock syndrome toxin (TSST-1) and enterotoxin C3, confirming the potential of

188 in vitro, while toxic shock syndrome toxin (TSST-1) exhibited increased movement at lower doses.

189 mmunity-associated (CA) MRSA strains USA200 (TSST-1(+)), MW2 (SEC(+)), c99-529 (SEB(+)), or purified

190 9 S. aureus isolates recovered, 14 (9%) were TSST-1 positive (12 unique strains).

191 responses induced by PWM were restored while TSST-1 induced responses remained inhibited.

192 The prevalences of colonization with TSST-1-producing S. aureus were comparable in Japan and

193 thal LPS hypersensitivity when injected with TSST-1, and these agents reduced the enhancement effect

194 All patients with TSST-1+ S aureus had overexpansion of V beta Z in blood

195 e pollen allergen season and stimulated with TSST-1, a prototypic superantigen.