PMID- 7768593
OWN - NLM
STAT- MEDLINE
DCOM- 19950705
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 63
IP  - 6
DP  - 1995 Jun
TI  - A toxic shock syndrome toxin 1 mutant that defines a functional site critical for 
      T-cell activation.
PG  - 2141-6
AB  - Toxic shock syndrome toxin 1 (TSST-1), a superantigen produced by Staphylococcus 
      aureus, is a causative agent of toxic shock syndrome (TSS). This superantigen is 
      a potent stimulator of T cells and macrophages/monocytes, resulting in the 
      release of cytokines that are implicated in the pathogenesis of TSS. This study 
      characterizes a mutant TSST-1, derived by site-directed mutagenesis, that has an 
      alanine substitution at histidine 135 (mutant 135). This single-amino-acid change 
      results in a mutant toxin that has lost mitogenic activity for T cells. In 
      contrast to wild-type TSST-1, this mutant does not induce T cells to express 
      interleukin-2, gamma interferon, or tumor necrosis factor beta (TNF-beta). The 
      inability of mutant 135 to activate T cells is not due to a lack of binding to 
      the class II major histocompatibility complex receptor. In addition, the mutant 
      TSST-1 does not induce expression of TNF-alpha, which plays a role in the 
      development of lethal shock. The lack of TNF-alpha induction by mutant 135 is 
      likely due to its inability to activate T cells. These data suggest that the 
      mutation at histidine 135 in TSST-1 affects toxin interactions with the T-cell 
      receptor rather than the class II major histocompatibility complex receptor.
FAU - Cullen, C M
AU  - Cullen CM
AD  - Department of Molecular Genetics, Biochemistry, and Microbiology, University of 
      Cincinnati College of Medicine, Ohio 45267, USA.
FAU - Blanco, L R
AU  - Blanco LR
FAU - Bonventre, P F
AU  - Bonventre PF
FAU - Choi, E
AU  - Choi E
LA  - eng
GR  - AI 30622/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Bacterial Toxins)
RN  - 0 (Enterotoxins)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Interleukin-2)
RN  - 0 (Superantigens)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (enterotoxin F, Staphylococcal)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - *Bacterial Toxins
MH  - Base Sequence
MH  - Enterotoxins/chemistry/*physiology
MH  - Histocompatibility Antigens Class II/metabolism
MH  - Interferon-gamma/biosynthesis
MH  - Interleukin-2/biosynthesis
MH  - *Lymphocyte Activation
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Staphylococcus aureus/*pathogenicity
MH  - Structure-Activity Relationship
MH  - Superantigens/*physiology
MH  - T-Lymphocytes/*immunology
MH  - Tumor Necrosis Factor-alpha/biosynthesis
PMC - PMC173278
EDAT- 1995/06/01 00:00
MHDA- 1995/06/01 00:01
PMCR- 1995/06/01
CRDT- 1995/06/01 00:00
PHST- 1995/06/01 00:00 [pubmed]
PHST- 1995/06/01 00:01 [medline]
PHST- 1995/06/01 00:00 [entrez]
PHST- 1995/06/01 00:00 [pmc-release]
AID - 10.1128/iai.63.6.2141-2146.1995 [doi]
PST - ppublish
SO  - Infect Immun. 1995 Jun;63(6):2141-6. doi: 10.1128/iai.63.6.2141-2146.1995.