ライフサイエンスコーパス: superantigen

1 ant T-cell receptor fragment and a bacterial superantigen.

2 ion against the debilitating effects of this superantigen.

3 to ubiquitously express a membrane-bound IgD-superantigen.

4 imulation in a manner reminiscent of a viral superantigen.

5 HC-T-cell receptor interactions and is not a superantigen.

6 death that is induced by a microbial B cell superantigen.

7 cal and behavioral effects attributed to the superantigen.

8 lls triggers the expression of an endogenous superantigen.

9 B. anthracis edema toxin against a bacterial superantigen.

10 I outside the groove, in a manner similar to superantigen.

11 he TCR with the staphylococcal enterotoxin B superantigen.

12 nt of the streptococcal pyrogenic exotoxin A superantigen.

13 rgy development in the presence of bacterial superantigen.

14 8 T cells downregulated CD244 in response to superantigen.

15 ymphocytes, which define the properties of a superantigen.

16 pUL32 is consistent with the properties of a superantigen.

17 a-chains reactive against several retroviral superantigens.

18 mammary tumor virus and herpesvirus saimiri superantigens.

19 MW2 (SEC(+)), c99-529 (SEB(+)), or purified superantigens.

20 nia after challenge with CA-MRSA or purified superantigens.

21 challenged intrabronchially with CA-MRSA or superantigens.

22 eta domains with a high affinity for binding superantigens.

23 treatment for diseases mediated by bacterial superantigens.

24 We determined vaginal Staphylococcus aureus superantigens.

25 to mount a potent T-cell immune response to superantigens.

26 also colonize the nasopharynx and elaborate superantigens.

27 nventional T cells to strong stimuli such as superantigens.

28 logy with the C-terminal domain of bacterial superantigens.

29 tribute to the general TCR binding for these superantigens.

30 l a role for B7-2 as obligatory receptor for superantigens.

31 in activity, and its activity is enhanced by superantigens.

32 ed respiratory syncytial virus and bacterial superantigens.

33 responsive to endogenous retrovirus-encoded superantigens.

34 The compound (20 microg/mL) prevented superantigen (100 microg/mL) induced cytokine secretion

35 GML (>or=10 microg/mL) inhibited superantigen (5 microg/mL) immunoproliferation, as deter

36 s, l-phytohemagglutin, Staphylococcus aureus superantigen, a superagonist anti-CD28 Ab, and in MLRs.

37 ctors, cytolysins, aid in the penetration of superantigens across vaginal mucosa as a representative

38 Rapid and robust adhesion of Tck and superantigen-activated T cells to FLS was observed that

39 pse microscopy, the interactions of resting, superantigen-activated, and cytokine-activated T cells w

40 In this report, we demonstrate the superantigen activity of HERV-K18 Env in mice and descri

41 B cell superantigen activity through affinity for BCR carbohydr

42 via coagulases and protein A-mediated B cell superantigen activity, are discussed as possible vaccine

43 (H)3-type B cell receptors to trigger B cell superantigen activity.

44 al for implementing peptidoglycan-linked SpA superantigen activity.

45 site for TRIM21 PRYSPRY reveals TRIM21 as a superantigen analogous to bacterial protein A and sugges

46 e genes included the gene coding for the MAM superantigen and genes coding for ribosomal proteins S15

47 cted with staphylococcal enterotoxin B (SEB) superantigen and H57-597 mAb, the expansion of SEB-react

48 Virulence factors include a superantigen and membrane adhesins and possibly also a b

49 tor-mediated stimulation when triggered by a superantigen and non-VSMC target cells.

50 islands (SaPIs), which carry and disseminate superantigen and other virulence genes.

51 lococcal pathogenicity islands (SaPIs) carry superantigen and resistance genes and are extremely wide

52 primes human MCs to activate T cells through superantigen and to present CMV antigen to TH1 cells, co

53 tivation of T cells by Staphylococcus aureus superantigen and, when preincubated with CMV antigens, i

54 Active vaccination against secreted superantigens and cytolysins resulted in protection of 8

55 Here we show that superantigens and cytolysins, when used in vaccine cockt

56 bacterial survival, including those encoding superantigens and host-evasion proteins regulated by a m

57 R2 messenger RNA neosynthesis, by a range of superantigens and superantigen-containing Streptococcus

58 interaction between gram-positive bacterial superantigens and toll-like receptor 2 (TLR2) in health

59 Several staphylococcal exotoxins can act as superantigens and/or antigens in models of atopic dermat

60 th staphylococcal enterotoxin B, a pyrogenic superantigen, and their inflammatory responses were asse

61 Cytolysins, superantigens, and proteases were identified as potentia

62 nd cytolysins (alpha-toxin and gamma-toxin), superantigens, and proteases were identified as the majo

63 Using superantigen- and tumor-induced anergy models, we found

64 ecognize a peripherally expressed endogenous superantigen are tolerized either by deletion or TCR rev

65 gm in which in vivo encounters with a B cell superantigen are uniformly associated with proliferative

66 Superantigens are a class of proteins that are derived f

67 Superantigens are immune-stimulatory toxins produced by

68 Due to high stability and toxicity, superantigens are potential agents of bioterrorism.

69 A group of virulence factors known as superantigens are produced by both of these organisms th

70 We also demonstrate that superantigens are solely responsible for monocyte TLR4 u

71 Superantigens are toxins produced by Staphylococcus aure

72 e specific for a mouse endogenous retroviral superantigen, become activated and proliferate in respon

73 re with reduction of Vkappa that contain the superantigen binding motif in all exposed mice.

74 peptides bind diverse superantigens, prevent superantigen binding to cell-surface B7-2 or CD28, atten

75 n for BALB/c mice, consistent with bacterial superantigens binding more efficiently to human than mur

76 ly stage of the pathogenic process, when the superantigen binds to its receptor, could limit the seve

77 We found that although all superantigens bound rapidly to the surface of human B ce

78 a chain activation was consistent with known superantigens, but deletion of SelX or SEK and SEQ was n

79 ter with a peripherally expressed endogenous superantigen by undergoing either deletion or TCR revisi

80 o a family of bacterial proteins that act as superantigens by activating a large subset of the T-cell

81 ome toxin 1 (TSST-1), enterotoxin, and other superantigens by coagulase-negative staphylococci, no as

82 Pattern recognition of bacterial superantigens by MHC class II receptors may exacerbate t

83 s aureus secretes various toxins that act as superantigens by stimulating a large fraction of the hos

84 ddition to canonical Lck-PLCgamma signaling, superantigens can activate a noncanonical G protein-PLCb

85 Staphylococcal superantigens cause toxic shock syndrome, which is chara

86 ted chronic intranasal exposure to bacterial superantigens causes airway inflammation and systemic im

87 overexpression, and protect mice from lethal superantigen challenge.

88 th major histocompatibility complex class II-superantigen complexes.

89 eosynthesis, by a range of superantigens and superantigen-containing Streptococcus pyogenes supernata

90 Superantigens contribute to lethal pulmonary illnesses d

91 Rabbits challenged with CA-MRSA or superantigens developed fatal, pulmonary illnesses.

92 antigens in vivo as activation of T cells by superantigens does not require CD4 and CD8 coreceptors.

93 In the liver, kappa cells recognized superantigen, down-regulated surface Ig, and expressed a

94 nking in the absence of complementarity is a superantigen effect induced by some microbial products t

95 d to an endogenous mouse mammary tumor virus superantigen either by deletion or TCR revision.

96 By binding CD28, bacterial superantigens elicit harmful inflammatory cytokine overe

97 L/6J mice undergo tolerance to an endogenous superantigen encoded by mouse mammary tumor virus 8 (Mtv

98 In contrast to results from animal models, superantigen-endotoxin interaction was not dependent on

99 12-aa beta-strand-hinge-alpha-helix domain, superantigens engage both B7-2 and CD28 at their homodim

100 ittle is known regarding the pathogenesis of superantigens entering through the intranasal route.

101 d by acute challenge with the staphylococcal superantigen enterotoxin B were comparable between WT an

102 ll-targeted properties of a microbial B cell superantigen, even at submicrogram doses associated with

103 Unlike the acute effects of superantigen exotoxins absorbed through the gut or vagin

104 S. aureus can elaborate a variety of superantigen exotoxins in "carrier" or "pathogenic" stat

105 In superantigen-expressing mice, as well as in mice carryin

106 The biological significance of this superantigen expression for the EBV life cycle is discus

107 Superantigens fall into two groups: superantigens such a

108 dis-derived mitogen (MAM) is a member of the superantigen family that structurally differs from other

109 t of the IgH, indicating that protein L is a superantigen for IGLV3-21-encoded lambda-IgL.

110 Protein L (PpL) is a B-cell superantigen from Peptostreptococcus magnus known to bin

111 ressing a membrane-tethered gamma2a-reactive superantigen (gamma2a-macroself Ag) and assessed the fat

112 ncode a gene with similarity to a retroviral superantigen gene (sag) of the unrelated mouse mammary t

113 We show that custom superantigens generated by single chain antibody technol

114 strain 4047 with sequential deletion of the superantigen genes were generated.

115 lococcal pathogenenicity islands, containing superantigen genes, and other mobile elements transferre

116 aphylococcus aureus that carry tst and other superantigen genes.

117 IgH(a/b) mice carrying the superantigen had a approximately 50% loss in follicular

118 The M. arthritidis mitogen (MAM) superantigen has long been implicated as having a role i

119 acids F119-D130), relatively conserved among superantigens, has been implicated in superantigen penet

120 For this reason, superantigens have been implicated in the development of

121 event superantigen lethality by blocking the superantigen-host costimulatory receptor interaction.

122 IgM(b) superantigen hosts reconstituted with experimental bone

123 usly identified and cloned an EBV-associated superantigen, human endogenous retrovirus (HERV)-K18 env

124 Superantigen-immune animals or animals treated with solu

125 ot proliferate in response to the tolerizing superantigen, implicating TCR revision as a mechanism of

126 permit the investigation of the role of this superantigen in the life cycle of EBV and its implicated

127 D3/CD28 beads or dendritic cells pulsed with superantigen in the presence of pro-Th17 cytokines IL-1b

128 We investigated the role played by superantigens in lung-associated lethal illness in rabbi

129 erosol exposure and possibly other bacterial superantigens in the context of human MHC class II recep

130 indicates the involvement of staphylococcal superantigens in the pathophysiology of patients with se

131 se DNT cells could be activated by bacterial superantigens in vivo as activation of T cells by supera

132 Superantigens, including bacterial enterotoxins, are a f

133 be activated directly by a bacterial protein superantigen independent of CD1d but also indicate that

134 Thus, superantigens induce a cytokine storm not only by mediat

135 Superantigens induce a state of steroid resistance in ac

136 Here we show that bacterial superantigens induce rapid transcription and increased m

137 Superantigen-induced allergic inflammation was studied i

138 eficient B cells were protected from in vivo superantigen-induced death and instead underwent persist

139 al T cells, which is clearly demonstrated by superantigen-induced expansion and subsequent deletion o

140 that S. aureus also regulates the profile of superantigen-induced T cell recruitment.

141 These effects translated into inhibition of superantigen-induced Th1 cell recruitment.

142 d both alloantigen-induced proliferation and superantigen-induced transendothelial migration of memor

143 lyclonal activators such as bacteria-derived superantigens induces activation, proliferation, and apo

144 t to test the hypothesis that staphylococcal superantigen influences the allergen-specific T cell res

145 Superantigens interact with T cells and APCs to cause ma

146 Superantigens interact with T lymphocytes and macrophage

147 Bacterial superantigen intoxication causes massive overactivation

148 This superantigen is transactivated upon IFN-alpha treatment

149 igens M and N declined, but enterotoxin-like superantigens K, L, and Q increased.

150 Staphylococcal enterotoxin B (SEB) is a superantigen known to be a modulator of chronic airway i

151 SEB is one of the most potent superantigens known and treatment of SEB induced shock r

152 o the surface of human B cells, zinc-binding superantigens largely remained at the cell surface for a

153 B7-2 homodimer interface mimotopes prevent superantigen lethality by blocking the superantigen-host

154 data reconcilable with the hypothesis that a superantigen-like activation contributes to the maturati

155 th atopic dermatitis with regard to signs of superantigen-like activation, clonal relationship, and i

156 es identify a candidal protein that displays superantigen-like activities.

157 on of a viral pathogenecity determinant with superantigen-like activity for CD8(+) T cells broadens t

158 bound rabbit IgM through an unconventional, superantigen-like binding site, and in vivo, surface mol

159 B cell development in GALT may be driven by superantigen-like molecules, and furthermore, that bacte

160 tes a potent TLR2 antagonist, staphylococcal superantigen-like protein 3 (SSL3), which prevents recep

161 ates virulence genes, including a hemolysin, superantigen-like protein, and phenol-soluble modulin, a

162 ulatory proteins known as the staphylococcal superantigen-like proteins (Ssls) under conditions of po

163 mmunomodulators, known as the staphylococcal superantigen-like proteins (Ssls), is mediated by the ma

164 ing method based on genes encoding S. aureus superantigen-like proteins, which belong to a family of

165 ells responded digitally to stimulation with superantigen-loaded antigen-presenting cells, whereas th

166 Enterotoxins G and I and enterotoxin-like superantigens M and N declined, but enterotoxin-like sup

167 I binding site of the Mycoplasma arthritidis superantigen MAM.

168 he devastating systemic effects of bacterial superantigens may be explained by powerful proinflammato

169 ly in vivo and chronic exposure to bacterial superantigens may precipitate a lupus-like autoimmune di

170 Toxic shock syndrome (TSS) and other superantigen-mediated illnesses are associated with 'sys

171 nstitute an attractive therapeutic target in superantigen-mediated illnesses.

172 We show that because of an apparent superantigen-mediated loss of naive Vbeta5(+) Tg CD4(+)

173 molecules and thus should not be subject to superantigen-mediated negative selection.

174 Because HLA class II molecules present superantigens more efficiently than murine MHC class II

175 ns localized at the vaginal surface, and the superantigen must therefore penetrate the vaginal mucosa

176 Superantigen mutant constructs with disrupted major hist

177 genes supernatants, although not by isogenic superantigen-negative strains.

178 SEA and other zinc-dependent, cross-linking superantigens on the surface of antigen-presenting cells

179 not dependent on T-cell receptor ligation by superantigen or interferon gamma production.

180 express CD25 and proliferate when exposed to superantigen or to cytomegalovirus (CMV) antigen using m

181 purified monocytes were exposed to purified superantigens or isogenic bacterial supernatants and rea

182 Some rabbits were preimmunized against superantigens or treated with soluble high-affinity T ce

183 Animals preimmunized against purified superantigens, or treated passively with Vbeta-TCRs and

184 Two separate models of superantigen penetration are proposed: staphylococcal al

185 among superantigens, has been implicated in superantigen penetration of the epithelium.

186 orcine vaginal mucosa in an ex vivo model of superantigen penetration.

187 ly CD28 but also its coligand B7-2 directly, superantigens potently enhance the avidity between B7-2

188 ation (TEM) in response to TCR engagement by superantigen presented by the ECs, leaving intact chemok

189 of iNKT cells involving a microbial protein superantigen presented in the context of major histocomp

190 imer interface mimetic peptides bind diverse superantigens, prevent superantigen binding to cell-surf

191 sses due to CA-MRSA; preexisting immunity to superantigens prevents lethality.

192 ther Vbeta-bearing T cells by staphylococcal superantigens prior to neoplastic transformation, result

193 er, our data may explain why colonization of superantigen-producing S. aureus can induce, under some

194 However, superantigen-producing Staphylococcus aureus strains are

195 f virulence factors including staphylococcal superantigens, proteases, and leukotoxins, in addition t

196 e host immune system of exposure to a B cell superantigen, protein L (PpL), a product of the common c

197 rected to amyloid beta peptide and microbial superantigen proteins.

198 dynamic in T-cells activated by contact with superantigen pulsed B-cells and could move from the dist

199 rmation between CD4(+)KIR2DL2(+) T cells and superantigen-pulsed target cells or the development of m

200 ly expressed kappa-macroself Ag, a synthetic superantigen reactive to Igkappa.

201 ne system, mice were engineered to express a superantigen reactive to IgM of allotype b (IgM(b)).

202 sible for the toxic shock syndrome and other superantigen-related diseases.

203 Whether this is indicative of all T-cell superantigens remains to be determined, although it stan

204 ulti-drug resistance and expression of a new superantigen repertoire in the M1T1 clone should trigger

205 an internal control mechanism that maintains superantigen responses within a defined range, which hel

206 group A Streptococcus pyogenes (GAS) express superantigen (SAg) exotoxin proteins capable of inducing

207 oxp3(+) Treg that is dependent on retroviral superantigen (sag) genes encoded in the mouse genome.

208 exogenous C3H MMTV infection, preventing the superantigen (Sag) response and mammary tumorigenesis.

209 coccus aureus, a primary source of bacterial superantigen (SAg), is known to colonize the human respi

210 Although in vivo virus superantigen (Sag)-mediated activation of T cells was si

211 Chronic nasal and skin colonization with superantigen (SAg)-producing Staphylococcus aureus is we

212 Of these exotoxins, the superantigens (SAg) are likely most pathogenic because o

213 Superantigens (SAgs) are causative in many S. aureus inf

214 Superantigens (SAgs) are potent exotoxins secreted by St

215 occus aureus and Streptococcus pyogenes, the superantigens (SAgs) are the most potent T-cell activato

216 Superantigens (SAGs) bind simultaneously to major histoc

217 Microbial products serving as superantigens (SAgs) have been implicated in triggering

218 gest that T(regs) are induced by exposure to superantigens (SAgs) in vitro or in vivo.

219 Superantigens (SAGs) interact with host immune receptors

220 Superantigens (SAgs) play an important role in the patho

221 s caused by staphylococcal and streptococcal superantigens (SAgs) that provoke a swift hyperinflammat

222 e stimulated with a mixture of streptococcal superantigens (SAgs), secreted by the prevalent M1T1 str

223 Staphylococcal superantigens (SAgs), such as toxic shock syndrome toxin

224 es potent immunomodulatory proteins known as superantigens (SAgs), which engage lateral surfaces of m

225 ative of a new class of antigens, the B-cell superantigens (SAgs).

226 recently acquired phage-associated bacterial superantigens (sAgs; SeeH, SeeI, SeeL, and SeeM) that sh

227 al peptides EBNA1 and BZLF1 or the bacterial superantigen SEB by flow cytometry.

228 Being a superantigen, SEB initiates an exaggerated inflammatory

229 Examination of the structure of the superantigen SEC2 bound to the beta-chain of a T-cell re

230 In general, superantigen-secreting S. aureus remains localized at th

231 The staphylococcal superantigen SEE induced the production of Th1 cell-recr

232 pproaches, we generated iNKT cell-deficient, superantigen-sensitive HLA-DR4-transgenic (DR4tg) mice,

233 , including IgE antibodies to staphylococcal superantigens; several studies using biologic agents hav

234 Such engineered superantigens should prove useful as reagents in immunoc

235 ixed peripheral blood mononuclear cells with superantigens significantly enhanced the induction of pr

236 riophage-encoded determinants DNase Sda1 and superantigen SpeA2 contributing to enhanced virulence an

237 n and the presence of S. aureus enterotoxin (superantigen)-specific IgE in the nasal polyp mucosa.

238 ic B cells can mediate negative selection of superantigen-specific, self-reactive, single-positive th

239 ing protein (SfbX49), and a prophage-encoded superantigen, SpeH.

240 mobile genetic elements confer expression of superantigens SSA and SpeC, and resistance to tetracycli

241 tance, and prophage PhiHKU.vir, encoding the superantigens SSA and SpeC, as well as the DNase Spd1.

242 ND.4, harboring genes encoding streptococcal superantigen (ssa), streptococcal pyrogenic exotoxins (s

243 ansient conjugation times in response to the superantigen staphylococcal enterotoxin A on dendritic c

244 The bacterial superantigen staphylococcal enterotoxin B (SEB) interact

245 ctival exposure to the Staphylococcus aureus superantigen staphylococcal enterotoxin B (SEB) may occu

246 nt-induced survival after challenge with the superantigen staphylococcal enterotoxin B (SEB), using l

247 otein consisting of a mutated variant of the superantigen staphylococcal enterotoxin E (SEA/E-120) li

248 ein and neutralized the clinically important superantigens staphylococcal enterotoxin B and TSS toxin

249 al T cells, which is clearly demonstrated by superantigen (staphylococcal enterotoxin B)-induced dele

250 sence of protein kinase C-theta (PKC-theta), superantigen (staphylococcal enterotoxin B)-induced dele

251 exotoxins of Gram-positive bacteria, such as superantigens [staphylococcal enterotoxins, toxic shock

252 in lymph node cells of mice immunized with a superantigen, staphylococcal enterotoxin B.

253 to investigate the potential role played by superantigens, staphylococcal enterotoxin B (SEB), staph

254 LPS induced long-term survival of superantigen-stimulated CD4 and CD8 T cells in a MyD88-d

255 a signaling in T cell activation and renders superantigen-stimulated T cells insensitive to glucocort

256 SMZL lymphomagenesis involves antigen and/or superantigen stimulation and molecular deregulation of g

257 (+) T cells respond to peripheral endogenous superantigen stimulation by undergoing deletion or TCR r

258 ace, where they could mediate staphylococcal superantigen stimulation of T cells.

259 sis by modulating responses to streptococcal superantigens (Strep-SAgs).

260 iferative responses to PHA and streptococcal superantigen, streptococcal pyrogenic exotoxin.

261 ty complex class II (MHC-II) and more potent superantigens such as SEA with a second, zinc-dependent

262 Superantigens fall into two groups: superantigens such as staphylococcal enterotoxin B (SEB)

263 hnology can be used to study the activity of superantigens such as toxic shock syndrome toxin 1 and a

264 eta-TCRs and then challenged with CA-MRSA or superantigens, survived.

265 e expressing an Igkappa-light chain-reactive superantigen targeted to the plasma membrane of hepatocy

266 ylococcal enterotoxin A (SEA) is a microbial superantigen that activates T-lymphocytes and induces pr

267 ylococcal enterotoxin B (SEB) is a bacterial superantigen that binds the receptors in the APC/T cell

268 lasma arthritidis-derived mitogen (MAM) is a superantigen that can activate large fractions of T cell

269 lasma arthritidis-derived mitogen (MAM) is a superantigen that can activate large fractions of T cell

270 aphylococcal enterotoxin B (SEB) is a potent superantigen that contributes to its virulence.

271 ential biological warfare agent, is a potent superantigen that contributes to the virulence of methic

272 Staphylococcal enterotoxin B (SEB) is a superantigen that cross-links the major histocompatibili

273 ylococcal enterotoxin B (SEB) is a bacterial superantigen that engages the immune system in a T-lymph

274 envelope (Env) protein of HERV-K18 encodes a superantigen that strongly stimulates a large number of

275 on accurately predicted mAb binding to other superantigens that share conformational epitopes with SE

276 ibility complex [MHC] class II molecules and superantigens), the S. aureus Eap protein does not block

277 l downregulates the human T cell response to superantigens through a TLR2-dependent, IL-10-mediated m

278 ns in the conventional manner to CDRs and as superantigens to framework regions of anti-SEE IgE in an

279 Administration of the superantigen toxic shock syndrome toxin 1 (TSST-1) resul

280 The staphylococcal superantigen toxic shock syndrome toxin-1 (TSST-1) is a

281 Staphylococcus aureus superantigen toxic shock syndrome toxin-1 is a major cau

282 Some strains of S. aureus produce the superantigen toxic shock syndrome toxin-1, which can pen

283 (hyperimmune serum) against combinations of superantigens (toxic shock syndrome toxin 1, enterotoxin

284 slands in staphylococci that carry genes for superantigen toxins and other virulence factors and are

285 icity islands (SaPIs), which carry genes for superantigen toxins and other virulence factors.

286 netic element that carries genes for several superantigen toxins.

287 During toxic shock syndrome (TSS), bacterial superantigens trigger a polyclonal T -cell response lead

288 In contrast to mice expressing kappa superantigen ubiquitously, in which kappa cells edit eff

289 Superantigens up-regulate monocyte surface TLR2 expressi

290 Mouse mammary tumor virus superantigens (vSAGs) are notorious for defying structur

291 Contamination of extracts with endotoxin or superantigen was excluded.

292 domain of a T cell receptor and a bacterial superantigen, we find that combinations of mutations fro

293 IgM(b/b) mice carrying superantigen were severely B cell lymphopenic, but small

294 Superantigens were administered intranasally on multiple

295 In contrast, single-binding-site superantigens were greatly depleted from the surface by

296 l as (but no higher than) that seen when the superantigens were presented by the high-risk alleles.

297 o a level comparable to that seen when these superantigens were presented by the protective HLA-II al

298 helial cells demonstrated that although both superantigens were proinflammatory, only the staphylococ

299 Superantigens were unable to signal through ligation by

300 Our results suggest that superantigens with improved affinity and/or specificity