ライフサイエンスコーパス: superantigen

1 rgy development in the presence of bacterial superantigen.

2 8 T cells downregulated CD244 in response to superantigen.

3 ymphocytes, which define the properties of a superantigen.

4 pUL32 is consistent with the properties of a superantigen.

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

6 ion against the debilitating effects of this superantigen.

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

8 imulation in a manner reminiscent of a viral superantigen.

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

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

11 cal and behavioral effects attributed to the superantigen.

12 lls triggers the expression of an endogenous superantigen.

13 B. anthracis edema toxin against a bacterial superantigen.

14 t description of a thiol-activated bacterial superantigen.

15 he TCR with the staphylococcal enterotoxin B superantigen.

16 nt of the streptococcal pyrogenic exotoxin A superantigen.

17 ed respiratory syncytial virus and bacterial superantigens.

18 responsive to endogenous retrovirus-encoded superantigens.

19 a-chains reactive against several retroviral superantigens.

20 mammary tumor virus and herpesvirus saimiri superantigens.

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

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

23 challenged intrabronchially with CA-MRSA or superantigens.

24 eta domains with a high affinity for binding superantigens.

25 treatment for diseases mediated by bacterial superantigens.

26 We determined vaginal Staphylococcus aureus superantigens.

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

28 also colonize the nasopharynx and elaborate superantigens.

29 nventional T cells to strong stimuli such as superantigens.

30 tribute to the general TCR binding for these superantigens.

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

32 -neutralizing activity against streptococcal superantigens.

33 in activity, and its activity is enhanced by 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 s that restrict S. aureus growth and inhibit superantigen-activated T cells but also by limiting NK c

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

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

41 disease exhibit TCR skewing consistent with superantigen activation.

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

43 B cell superantigen activity through affinity for BCR carbohydr

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

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

46 al for implementing peptidoglycan-linked SpA superantigen activity.

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

48 ilk but not bovine milk or formula inhibited superantigen and bacterial-induced IL-8 production by mo

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

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

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

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

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

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

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

56 R Vbeta2-specific, TNF-dominated response to superantigens and a later IL-12- and IL-18-dependent, IF

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

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

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

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

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

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

63 es also limit T cell activation by S. aureus superantigens, and EPS abrogates systemic induction of g

64 Cytolysins, superantigens, and proteases were identified as potentia

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

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

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

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

69 Superantigens are a class of proteins that are derived f

70 Superantigens are immune-stimulatory toxins produced by

71 GAS superantigens are key mediators of STSS through their po

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

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

74 Superantigens are toxins produced by Staphylococcus aure

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

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

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

78 een reported to affect antibody receptor and superantigen binding; however, such effects in IgE remai

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

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

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

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

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

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

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

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

87 Staphylococcal superantigens cause toxic shock syndrome, which is chara

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

89 overexpression, and protect mice from lethal superantigen challenge.

90 th major histocompatibility complex class II-superantigen complexes.

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

92 Superantigens contribute to lethal pulmonary illnesses d

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

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

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

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

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

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

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

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

101 12-aa beta-strand-hinge-alpha-helix domain, superantigens engage both B7-2 and CD28 at their homodim

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

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

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

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

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

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

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

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

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

111 come the limitation of conventional antibody-superantigen fusion proteins, we have split a superantig

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

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

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

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

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

117 aphylococcus aureus that carry tst and other superantigen genes.

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

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

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

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

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

123 IgM(b) superantigen hosts reconstituted with experimental bone

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

125 Superantigen-immune animals or animals treated with solu

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

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

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

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

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 We discovered that S. aureus uses a rapid, superantigen-independent mechanism to induce host IFN-ga

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

136 Superantigens induce a state of steroid resistance in ac

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 ough reactive oxygen species and to limiting superantigen-induced T cell activation and interferon ga

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

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

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

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

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

146 Superantigens interact with T cells and APCs to cause ma

147 Superantigens interact with T lymphocytes and macrophage

148 uperantigen fusion proteins, we have split a superantigen into two fragments, individually inactive,

149 This superantigen is transactivated upon IFN-alpha treatment

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

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

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

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 screte binding modalities: a non-clonotypic, superantigen-like interaction mediating subset-specific

160 though many questions remain unanswered, one superantigen-like modality features interactions of germ

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

162 Here we show Staphylococcal Superantigen-Like protein 11 (SSL11) from MRSA USA300_FP

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

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

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

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

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

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

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

170 I binding site of the Mycoplasma arthritidis superantigen MAM.

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

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

173 ent, nonclonal T cell responses to microbial superantigens may reflect subversion of physiologic inna

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

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

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

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

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

179 Superantigen mutant constructs with disrupted major hist

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 However, superantigen-producing Staphylococcus aureus strains are

196 TSS) is a life-threatening disease caused by superantigen-producing Staphylococcus aureus.

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

198 onRIalpha, anti-IgE omalizumab, antigen, and superantigen protein A (spA) by using the pertuzumab and

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

200 rected to amyloid beta peptide and microbial superantigen proteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 Superantigens (SAgs) are potent exotoxins secreted by St

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

218 Superantigens (SAGs) bind simultaneously to major histoc

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

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

221 Superantigens (SAGs) interact with host immune receptors

222 Superantigens (SAgs) play a major role in the pathogenes

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

224 Superantigens (SAgs) released by common Gram-positive ba

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

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

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

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

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

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

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

232 Being a superantigen, SEB initiates an exaggerated inflammatory

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

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

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

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

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

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

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

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

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

242 ng prophage PhiHKU.vir encoding the secreted superantigens SSA and SpeC and the DNase Spd1.

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

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

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

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

247 The bacterial superantigen staphylococcal enterotoxin B (SEB) interact

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

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

250 both sequence and structure to the bacterial superantigen staphylococcal enterotoxin B.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 data suggest that SARS-CoV-2 S may act as a superantigen to trigger the development of MIS-C as well

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

281 nse triggered upon the binding of pathogenic superantigens to T cell receptors (TCRs) and/or major hi

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

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

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

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

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

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

288 netic element that carries genes for several superantigen toxins.

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

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

291 Superantigens up-regulate monocyte surface TLR2 expressi

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

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

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

295 Superantigens were administered intranasally on multiple

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 t potent activators of T cells are bacterial superantigens, which bind to major histocompatibility co