HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
about
Sequences in both class II major histocompatibility complex alpha and beta chains contribute to the binding of the superantigen toxic shock syndrome toxin 1PI3K/Akt/mTOR, a pathway less recognized for staphylococcal superantigen-induced toxicityVirus-encoded superantigensCutaneous squamous cell cancer (cSCC) risk and the human leukocyte antigen (HLA) system.Clinical, microbial, and biochemical aspects of the exfoliative toxins causing staphylococcal scalded-skin syndrome.Staphylococcus-mediated T-cell activation and spontaneous natural killer cell activity in the absence of major histocompatibility complex class II molecules.Superantigens: mechanisms by which they may induce, exacerbate and control autoimmune diseases.Recombinant Staphylococcus aureus exfoliative toxins are not bacterial superantigensStaphylococcal enterotoxins bind H-2Db molecules on macrophagesSimilar cytokine induction profiles of a novel streptococcal exotoxin, MF, and pyrogenic exotoxins A and B.Binding and activation of major histocompatibility complex class II-deficient macrophages by staphylococcal exotoxins.Bacterial superantigens.Retroviral super-antigens and T cells.Allelic polymorphisms at the H-2A and HLA-DQ loci influence the response of murine lymphocytes to the Mycoplasma arthritidis superantigen MAM.Interaction of staphylococcal toxic shock syndrome toxin-1 and enterotoxin A on T cell proliferation and TNFα secretion in human blood mononuclear cells.Bacterial toxin-induced cytokine production studied at the single-cell level.Evidence that the murine AIDS defective virus does not encode a superantigen.Shared promoter elements between a viral superantigen and the major histocompatibility complex class II-associated invariant chain.Analysis of the interaction site for the self superantigen Mls-1a on T cell receptor V beta.Analysis of T cell stimulation by superantigen plus major histocompatibility complex class II molecules or by CD3 monoclonal antibody: costimulation by purified adhesion ligands VCAM-1, ICAM-1, but not ELAM-1.Dendritic cells are potent antigen-presenting cells for microbial superantigensIdentification of HLA-DR1 beta chain residues critical for binding staphylococcal enterotoxins A and E.Mutations defining functional regions of the superantigen staphylococcal enterotoxin B.Major histocompatibility complex-specific recognition of Mls-1 is mediated by multiple elements of the T cell receptor.T cell receptor interaction with peptide/major histocompatibility complex (MHC) and superantigen/MHC ligands is dominated by antigen.Small amounts of superantigen, when presented on dendritic cells, are sufficient to initiate T cell responses.Monoclonal antibodies defining functional sites on the toxin superantigen staphylococcal enterotoxin BT cell receptor-major histocompatibility complex class II interaction is required for the T cell response to bacterial superantigens.Major histocompatibility complex class II-associated peptides control the presentation of bacterial superantigens to T cells.Transcytosis of staphylococcal superantigen toxins.Mycoplasma superantigen is a CDR3-dependent ligand for the T cell antigen receptor.A mutational analysis of the binding of staphylococcal enterotoxins B and C3 to the T cell receptor beta chain and major histocompatibility complex class II.Sensitive, Rapid, Quantitative and in Vitro Method for the Detection of Biologically Active Staphylococcal Enterotoxin Type E.Influence of major histocompatibility complex haplotype on the mitogenic response of T cells to staphylococcal enterotoxin B.Selective manipulation of the human T-cell receptor repertoire expressed by thymocytes in organ cultureStimulated nuclear translocation of NF-kappaB and shuttling differentially depend on dynein and the dynactin complexUpdate on staphylococcal superantigen-induced signaling pathways and therapeutic interventions.Distinct binding sites on HLA-DR for invariant chain and staphylococcal enterotoxins.Expression of bacterial superantigen genes in mice induces localized mononuclear cell inflammatory responses.Effective activation alleviates the replication block of CCR5-tropic HIV-1 in chimpanzee CD4+ lymphocytes.
P2860
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P2860
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
description
1990 nî lūn-bûn
@nan
1990年の論文
@ja
1990年学术文章
@wuu
1990年学术文章
@zh-cn
1990年学术文章
@zh-hans
1990年学术文章
@zh-my
1990年学术文章
@zh-sg
1990年學術文章
@yue
1990年學術文章
@zh
1990年學術文章
@zh-hant
name
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@ast
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@en
type
label
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@ast
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@en
prefLabel
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@ast
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@en
P2093
P2860
P356
P1476
HLA-DR alleles differ in their ability to present staphylococcal enterotoxins to T cells.
@en
P2093
P2860
P304
P356
10.1084/JEM.172.3.709
P407
P577
1990-09-01T00:00:00Z