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1 SpeA stimulates V beta 2.1, 12.2, 14.1, and 15.1-positiv
3 such as streptococcal pyrogenic exotoxin A (SpeA) and SpeK, streptococcal superantigen (SSA), and a
4 s and to streptococcal pyrogenic exotoxin A (SpeA) and streptococcal superantigen (SSA) of Streptococ
5 en (SAg) streptococcal pyrogenic exotoxin A (SpeA) could be simulated, as determined by studying mult
8 rantigen streptococcal pyrogenic exotoxin A (SpeA) is associated with outbreaks of streptococcal toxi
9 produce streptococcal pyrogenic exotoxin A (SpeA), a bacterial superantigen capable of stimulating h
10 ting SAg streptococcal pyrogenic exotoxin A (SpeA), or active immunization with either wild-type or a
11 ssion of streptococcal pyrogenic exotoxin A (SpeA; also known as scarlet fever or erythrogenic toxin
13 erotoxins, toxic-shock syndrome toxin 1, and SpeA with antiserum prepared against HisSEG and HisSEI r
15 n 30 min of incubation with rSpeB, SpeG, and SpeA were more resistant and SpeJ was completely unaffec
16 were undertaken to determine regions of both SpeA and the TCR involved in the formation of MHC/SpeA/T
17 lonal M1T1 isolates expressing no detectable SpeA were inoculated into the implanted chambers, and th
19 e immunization, or vaccination with inactive SpeA, resulted in high-titer SpeA-specific antibodies in
20 the previously sequenced M1 genome including SpeA and another bacteriophage-encoded novel streptodorn
21 pyogenes lineage characterised by increased SpeA production has emerged during increased S pyogenes
24 ion with either wild-type or a nonfunctional SpeA mutant, protects mice from nasopharyngeal infection
26 he implanted chambers, and the expression of SpeA in the aspirated aliquots of the chamber fluid was
28 ewise, although the phenotypic expression of SpeA, SpeB, and SpeF proteins varied among the M1T1 isol
30 The analysis indicates that the residues of SpeA needed for a productive TCR interaction differ for
31 emporal relation between the upregulation of SpeA expression and the downregulation of SpeB expressio
32 teins, including the in vivo upregulation of SpeA, which occurred independently of SpeB inactivation.
33 mber and grown in vitro continued to produce SpeA even after 21 passages in vitro, suggesting stable
35 type (WT) strain, characterized by a SpeB(+)/SpeA(-)/Sda1(low) phenotype, and a hypervirulent animal-
38 selected for a stable phase-shift to a SpeB-/SpeA+ phenotype that expressed a full repertoire of secr
46 -IVIG plasma samples contained antibodies to SpeA, these antibodies did not block the activity of thi
48 n (HLA)-DQ8 rendered the mice susceptible to SpeA-induced lethal shock that was accompanied by massiv
50 ns of the V beta chains that interacted with SpeA, synthetic peptides representative of the human V b