ライフサイエンスコーパス: SpeA

1 SpeA stimulates V beta 2.1, 12.2, 14.1, and 15.1-positiv

2 strain: streptococcal pyrogenic exotoxin A (SpeA) and a streptodornase D (SdaD) homologue.

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

6 reactive streptococcal pyrogenic exotoxin A (SpeA) increased.

7 Streptococcal pyrogenic exotoxin A (SpeA) is a superantigen produced by Streptococcus pyogen

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 engineered non-SAg vaccine candidate against SpeA in the context of HLA.

12 erotoxins, toxic-shock syndrome toxin 1, and SpeA with antiserum prepared against HisSEG and HisSEI r

13 t length polymorphism (RFLP), M protein, and SpeA exotoxin sequence analyses.

14 n 30 min of incubation with rSpeB, SpeG, and SpeA were more resistant and SpeJ was completely unaffec

15 were undertaken to determine regions of both SpeA and the TCR involved in the formation of MHC/SpeA/T

16 lonal M1T1 isolates expressing no detectable SpeA were inoculated into the implanted chambers, and th

17 e immunization, or vaccination with inactive SpeA, resulted in high-titer SpeA-specific antibodies in

18 the previously sequenced M1 genome including SpeA and another bacteriophage-encoded novel streptodorn

19 and the TCR involved in the formation of MHC/SpeA/TCR complexes.

20 ion with either wild-type or a nonfunctional SpeA mutant, protects mice from nasopharyngeal infection

21 strains do not produce detectable amounts of SpeA in vitro.

22 he implanted chambers, and the expression of SpeA in the aspirated aliquots of the chamber fluid was

23 Expression of SpeA was detected in the chamber fluid as early as days

24 ewise, although the phenotypic expression of SpeA, SpeB, and SpeF proteins varied among the M1T1 isol

25 associated isolates is a more active form of SpeA.

26 The analysis indicates that the residues of SpeA needed for a productive TCR interaction differ for

27 emporal relation between the upregulation of SpeA expression and the downregulation of SpeB expressio

28 teins, including the in vivo upregulation of SpeA, which occurred independently of SpeB inactivation.

29 mber and grown in vitro continued to produce SpeA even after 21 passages in vitro, suggesting stable

30 We generated 20 mutant forms of SpeA1 (SpeA encoded by allele 1), and the mutant toxins were an

31 type (WT) strain, characterized by a SpeB(+)/SpeA(-)/Sda1(low) phenotype, and a hypervirulent animal-

32 r adapted to survive in vivo, with a SpeB(-)/SpeA(+)/Sda1(high) phenotype.

33 Injection of a SpeB+/SpeA- M1T1 GAS strain into a murine subcutanous chamber

34 selected for a stable phase-shift to a SpeB-/SpeA+ phenotype that expressed a full repertoire of secr

35 y of each to block proliferation, suggesting SpeA has distinct binding sites for the CDR loops.

36 The T-cell receptor (TCR)-SpeA interaction is crucial for superantigenic activity,

37 ns (CDRs) 1, 2, and 4 were used to block the SpeA-mediated proliferation of human PBMCs.

38 Phage T14 encodes the SpeA exotoxin and is closely related to the classic conv

39 Products of the SpeA and SpeB enzymes (agmatine and putrescine) were tes

40 athogenesis of STSS, we began studies on the SpeA-immune cell interaction.

41 n with inactive SpeA, resulted in high-titer SpeA-specific antibodies in vivo.

42 -IVIG plasma samples contained antibodies to SpeA, these antibodies did not block the activity of thi

43 SEG is most similar to SpeA, SEB, SEC, and SSA (38 to 42% amino acid identity),

44 n (HLA)-DQ8 rendered the mice susceptible to SpeA-induced lethal shock that was accompanied by massiv

45 Mice vaccinated with wild-type SpeA rendered Vbeta8(+) T cells poorly responsive, which

46 ns of the V beta chains that interacted with SpeA, synthetic peptides representative of the human V b