ArticleInfection and immunity1992
Dual roles for class II major histocompatibility complex molecules in staphylococcal enterotoxin-induced cytokine production and in vivo toxicity.
Article in Infection and immunity, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Enhancement of superantigen activity and antitumor response of staphylococcal enterotoxin C2 by site-directed mutagenesis.Cancer immunology, immunotherapy : CII · 2009Article
- Syndecan-1 is an in vivo suppressor of Gram-positive toxic shock.The Journal of biological chemistry · 2008Article
- Role of T cells and gamma interferon during induction of hypersensitivity to lipopolysaccharide by toxic shock syndrome toxin 1 in mice.Infection and immunity · 2001Article
- Mitogenic activities of amino acid substitution mutants of staphylococcal enterotoxin B in human and mouse lymphocyte cultures.Infection and immunity · 1996Article
- Bacterial modulins: a novel class of virulence factors which cause host tissue pathology by inducing cytokine synthesis.Microbiological reviews · 1996Review
- Biochemical and mutational analysis of the histidine residues of staphylococcal enterotoxin A.Infection and immunity · 1996Article
- A natural mutation of the amino acid residue at position 60 destroys staphylococcal enterotoxin A murine T-cell mitogenicity.Infection and immunity · 1995Article
- Bacterial pyrogenic exotoxins as superantigens.Clinical microbiology reviews · 1995Review
- A toxic shock syndrome toxin 1 mutant that defines a functional site critical for T-cell activation.Infection and immunity · 1995Article
- Modulins: a new class of cytokine-inducing, pro-inflammatory bacterial virulence factor.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 1995Review
- Langerhans' cell depletion by staphylococcal superantigens.Immunology · 1994Article
- Localization of binding sites of staphylococcal enterotoxin B (SEB), a superantigen, for HLA-DR by inhibition with synthetic peptides of SEB.Infection and immunity · 1994Article
- Similar cytokine induction profiles of a novel streptococcal exotoxin, MF, and pyrogenic exotoxins A and B.Infection and immunity · 1994Article
- Identification of staphylococcal enterotoxin B sequences important for induction of lymphocyte proliferation by using synthetic peptide fragments of the toxin.Infection and immunity · 1994Article
- Distribution and kinetics of superantigen-induced cytokine gene expression in mouse spleen.The Journal of experimental medicine · 1993Article
- Lack of complete correlation between emetic and T-cell-stimulatory activities of staphylococcal enterotoxins.Infection and immunity · 1993Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The staphylococcal enterotoxins (SE) specifically bind to class II major histocompatibility complex (MHC) proteins, resulting in activation of monocytes and T cells. The SE cause weight loss in mice, which is dependent on T-cell stimulation and tumor necrosis factor alpha (TNF-alpha) production. Here we use a mutant of staphylococcal enterotoxin A that binds class II MHC molecules and activates monocytes but not T cells to evaluate the relative contributions of monocyte- and T-cell-stimulatory activities to in vivo toxicity. The mutant toxin did not cause weight loss in B10. BR mice but did stimulate monocyte TNF-alpha production in vitro, as did the wild-type toxin. Addition of a supernatant from toxin-activated T cells enhanced monocyte-stimulatory activity of both mutant and wild-type toxins fivefold. The effect of the supernatant could be mimicked by recombinant gamma interferon (IFN-gamma) and was inhibited by antibody to IFN-gamma. These results suggest that toxin-induced monocyte TNF-alpha production is upregulated by IFN-gamma, which likely represents the T-cell requirement in SE-mediated weight loss. Our studies thus implicate two distinct class II MHC-dependent signaling pathways for SE, the first involving direct signal transduction through class II MHC molecules mediated by either mutant or wild-type toxin and the second requiring T-cell stimulation by toxin-class II MHC complexes with consequent production of IFN-gamma. We suggest that both pathways are required for optimal monocyte TNF-alpha production in vitro and SE-induced toxicity in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.