Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pyrogenic toxin (PT) family is composed of the staphylococcal enterotoxins (SE), the toxic shock syndrome toxin, and the streptococcal pyrogenic exotoxins (SPE). Whereas considerable effort has focused on characterization of PTs due to their unique biological properties, our understanding of the evolution of this gene family is incomplete. Phylogenetic relationships for members of the PT family were estimated by examining the previously reported nucleotide sequences of the genes encoding SPEA, SPEC, SEA, SEB, SEC1, SEC2, SEC3, SED, and SEE. Additionally, we present and analyze sequence data on seven previously unreported sec genes. Within the PT family, sequence divergence was partitioned in a hierarchical fashion such that mean sequence divergence ranged from 1.179 among all 16 toxin genes, 0.443 among those restricted to Staphylococcus, and 0.028 among the genes encoding 10 variants of Type C SE. Results of this study are interpreted as suggesting that the PT family consists of two large clades. One clade consists of the staphylococcal toxins SEA, SEE, and SED, being closely related to the streptococcal toxin SPEC, whereas the other clade depicts close relationships of the staphylococcal toxins SEC and SEB with the streptococcal toxin SPEA.
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PMID:Molecular evolution of the staphylococcal and streptococcal pyrogenic toxin gene family. 804 78

The RIDASCREEN SET kit (R-Biopharm GmbH, Darmstadt, Germany), a commercial staphylococcal enterotoxin (SE) visual immunoassay kit, was evaluated for its efficacy. The kit utilizes monovalent capture antibodies against SE types A to E (SEA to SEE); therefore, it simultaneously detects and identifies the enterotoxin types. The major advantages of the kit are (i) a high degree of specificity (except for naturally occurring peroxidases, food compositions or ingredients and microbiological products due to growth of nonstaphylococcal microorganisms did not cause false-positive results; additionally, no cross-reactions among reagents of the kits were observed), (ii) excellent sensitivity (minimum detectable limits were 0.20 to 0.30 ng of SEs per ml of extracts of ham, salami, and mushroom and 0.30 to 0.35 ng of SEs per ml of cheese extracts, or 0.50 to 0.75 ng of SEs per g of foods such as noodles, ham, salami, cheese, and turkey), (iii) simplicity (the kit enabled direct assay of SEs in food extracts without the need for lengthy extraction or concentration procedures), (iv) rapidity (it took less than 3 h to complete the analysis of individual enterotoxin types SEA to SEE), and (v) its semiquantitative results (optical density values could be read against a standard curve to estimate the amount of SE in the extract). The RIDASCREEN kit is a convenient, rapid, and reliable tool for the detection and identification of SEs in foods.
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PMID:Evaluation of a commercial enzyme immunoassay kit (RIDASCREEN) for detection of staphylococcal enterotoxins A, B, C, D, and E in foods. 813 22

The in vitro response of unprimed rat T cells to retroviral and bacterial superantigens (SAg) was analyzed with TCR V beta 8.2-, 8.5-, 10-, and 16-specific mAbs. Specific stimulation of V beta 8.2 and 8.5 CD4 cells was observed in the response to Mls1a, the retroviral SAg encoded by integrated provirus Mtv-7 (Mtv-7 SAg), which was presented by mouse B cells or mouse fibroblasts transfected with DR1 genes and the Mtv-7 SAg. Additionally, a strong response of V beta 16 CD4 cells to an as yet unidentified mouse SAg was found. Only some of the bacterial SAg known to stimulate mouse and human T cells also activated rat lymph node cells. SEA, SEE, and TSST-1 stimulated rat T cells well; SEB, SEC1, and SED did not. This defect was apparently a result of weak binding to rat MHC class II molecules because presentation by human MHC class II molecules restored T cell activation. Under these conditions, SEB stimulated V beta 8.2+ and 8.5+ CD4 and CD8 cells from Lewis rats. A comparison of several rat strains revealed an unresponsiveness to SEB or Mtv-7 SAg for V beta 8.2 cells from F344 and DA rats. Determination of the nucleotide sequences of the Tcrb-V8.2 of these strains revealed differences between SAg-responsive and SAg-unresponsive Tcrb-V8.2 in seven amino acids, four of them located in the putative SAg contact site. The significance of these findings for the evolution of TCR-SAg interactions is discussed.
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PMID:Control of the rat T cell response to retroviral and bacterial superantigens by class II MHC products and Tcrb-V8.2 alleles. 815 53

Overlapping peptides corresponding to the entire Nef (HIVBRU) sequence were tested for their relative abilities to block binding of staphylococcal enterotoxins (SEs) to Raji cells. An internal sequence, Nef(123-160), blocked binding of two highly homologous SEs, SEA and SEE, while it was less effective against SEB and SEC1. Nef(123-160) bound directly class II DR antigens, as assessed by specific antibodies, and its binding was significantly inhibited by SEE, and also by SEA to a lesser degree. Purified Nef inhibited specific binding of SEA to Raji cells in a dose-dependent manner. Nef induced IL 2 production and proliferation by human mononuclear cells. Definitive expansion of specific V beta T cell populations was not observed, possibly due to lesser mitogenic activity of Nef relative to SEs. Thus, Nef may have mitogenic activity similar to that of superantigens.
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PMID:Identification of an HIV-1 Nef peptide that binds to HLA class II antigens. 817 82

Staphylococcal enterotoxins (SEs) are known superantigens for T cells expressing the alpha beta T-cell receptor (TCR). They bind to MHC class II molecules on antigen-presenting cells and can subsequently trigger T-cell responses by binding to V beta-gene products. The reactivity of gamma delta T cells with enterotoxins is less well defined although both proliferative and cytotoxic responses have been described. In the present study we have tested the cytotoxic reactivity of a panel of 41 gamma delta T-cell clones against target cells coated with the enterotoxins SEA, SEB, SEC1, SEC2, SEC3, SED, SEE or TSST. Three reaction patterns were observed with the gamma delta T-cell clones: (1) clones that specifically lysed SEA-coated target cells only; (2) clones that specifically lysed SEE-coated target cells only, and (3) clones that specifically lysed SEA-coated target cells only in the presence of certain human sera. The presence of SEA-specific antibodies in such human sera could be demonstrated. Moreover, gamma delta T-cell clones of this third category expressed the IgG FcRIII (CD16) which indicates that these clones are capable of mediating antibody-dependent cellular cytotoxicity towards SEA-coated target cells. Thus, the cytotoxic response of gamma delta T cells to SEs is mediated by two distinct pathways: an antibody-independent and an antibody-dependent pathway. The antibody-independent reactivity of gamma delta T cells was directed to either SEA or SEE, whereas antibody-dependent reactivity was found only towards SEA. The capacity of gamma delta T-cell clones to respond to stimulation with SEs, combined with their high cytolytic capacity in vitro, suggests that these cells can be involved in SE-directed immune responses and efficiently kill SE-coated target cells in vivo.
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PMID:Reactivity of human gamma delta T cells to staphylococcal enterotoxins: a restricted reaction pattern mediated by two distinct recognition pathways. 832 63

We investigated the in vitro responsiveness of peripheral blood lymphocytes from two patients with T-cell chronic lymphocytic leukaemia (T-CLL) to Staphylococcus aureus enterotoxin (SE) superantigens. T-cell receptor (TcR) alpha beta (V beta 7.1)-expressing CD4+ leukaemic T cells from patient HE (white blood cell count 480,000/microliters) proliferated in response to SEA and, only at 1000-fold higher concentrations, to SEB, SED, and SEE. CD4+CD8+ TcR alpha beta (V beta 12.1)-expressing leukaemic T cells from patient KO (white blood cell count 120,000/microliters) were activated by SEB but not by the other tested SEs. In both instances, the activation of leukaemic T cells by SE was dependent on the presence of HLA-DR+ cells. Southern blot analysis of TcR beta gene rearrangement confirmed that the proliferating cells were derived from the leukaemic T-cell clone and not from contaminating normal T cells. These data indicate that leukaemic T cells from patients with T-CLL exert a clonally variable responsiveness to SE superantigens. We conclude that recognition of specific antigen and subsequent signal transduction can be initiated via the TcR of leukaemic T-CLL cells.
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PMID:Leukaemic T cells from patients with chronic lymphocytic leukaemia of T-cell origin respond to Staphylococcus aureus enterotoxin superantigens. 843 35

Human TCR gamma delta positive T cells can proliferate in response to stimulation with staphylococcal enterotoxins (SEs) or mediate lysis of SE pulsed target cells. In the small number of studies reported, the proliferative response of gamma delta T cells was limited to V gamma 9 negative cells and, in vitro, such responses do not require the presence of MHC class II molecules for antigen presentation. Proliferative responses have been found after stimulation with SEA, SEB and TSST. The cytolytic activity of gamma delta T cells can be mediated by two different mechanisms: either gamma delta T cells specifically interact with SEA pulsed target cells--this is most likely TCR mediated recognition--or gamma delta T cells mediate antibody dependent cellular cytotoxicity (ADCC). This latter reactivity depends on Fc-receptor expression by the gamma delta T cell clones and the presence of SE specific antibodies during the assay. So far cytotoxic gamma delta T cell reactivity has only been found against the highly homologous enterotoxins SEA and SEE. Finally, HLA-class II positive gamma delta T cell clones can present SE to other SE reactive T cells but appear to be relatively resistant to T cell mediated lysis. Taken together, TCR gamma delta positive T cells are able to respond to a number of bacterial superantigens and may therefore be involved in local immune responses to such antigens. This may be especially relevant for those gamma delta T cell subpopulations that are preferentially found in the (intestinal) epithelia where exposure to bacterial superantigens is likely to occur.
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PMID:Gamma delta T cell reactivity towards bacterial superantigens. 846 94

To investigate whether cell populations in CD3+ lymphoproliferative disease of granular lymphocytes (LDGLs) were skewed toward the use of specific V beta regions, we studied the repertoire of T-cell receptor (TCR) V beta gene products in 18 patients, as well as their relationship to the clonal bands in the Southern blot and the activation mediated by superantigens. Using a panel of monoclonal antibodies (mAbs) for conserved V beta segments and PCR, a dominant population expressing a specific V beta region was demonstrated in all patients. In five (27%) cases, granular lymphocytes (GLs) were found to express the V beta 13.1, while V beta 8 and V beta 6 were each expressed in three (17%) cases. The remaining cases were characterized by the proliferation of TCR V beta 2, V beta 3, V beta 4, V beta 9, V beta 12, V beta 16, and V beta 20. This finding indicates a biased usage of a limited TCR V beta in LDGLs, since nearly 60% of the cases utilized only three families of the TCR V beta genes. In all of the cases studied, we proved that the subset recognized by mAb and PCR was identical to that accounting for the extra band(s) of the Southern blot. This finding confirms the clonal nature of the population identified according to TCR V beta expression both by phenotype and PCR. On functional grounds, we evaluated whether GLs can be activated through the specific TCR using the superantigens recognizing discrete V beta families, such as staphylococcal proteins, including SEA, SEB, SEC1, SEC2, SED, and SEE. We demonstrated that the TCR-alpha/beta of clonal GLs in LDGL patients is functionally active in delivering cytotoxic and proliferative signals upon superantigen activation.
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PMID:Analysis of the T cell receptor in the lymphoproliferative disease of granular lymphocytes: superantigen activation of clonal CD3+ granular lymphocytes. 852 5

The study of the mouse T cell receptor (TcR) beta chain repertoire in BALB/c thymocytes led to the identification of the V beta 20 gene segment. The expression of V beta 20 estimated at the transcriptional level differs among mouse strains, suggesting clonal deletion. In the present study, we reconstituted by transfection functional TcR using the V beta 20 segment with different V alpha segments and studied the action of superantigen toxins. The V beta 20-transfectant T cells are activated by staphylococcal enterotoxins A and E (SEA and SEE) but not by the other tested toxins. The activation is dependent on the presence of cells expressing major histocompatibility complex class II molecules. Different HLA DR alleles can present the bacterial toxins, establishing that they interact with TcRV beta 20 as superantigens. Moreover, the V alpha domain associated with the V beta 20 domain has an influence on the response to these toxins. The fact that V beta 20 is recognized by SEA and SEE, although both toxins are known to interact with different sets of V beta, suggests the presence of different TcR binding sites on the toxins.
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PMID:Bacterial superantigen specificities of mouse T cell receptor V beta 20. 856 33

Staphylococcal enterotoxins (SE) bind to major histocompatibility complex (MHC) class II molecules and the V beta region of T cell receptors (TCR) and subsequently induces T cell proliferation. This mitogenicity is the basis of pathological effects seen in food poisoning and toxic shock syndrome. Toxin-specific monoclonal antibodies have previously been shown to be effective in blocking toxin stimulated T cell responses. In this study, a monoclonal antibody, 52BL1, was found to be a potent inhibitor of SEA-, SEB-, SEC1-, SED-, and SEE-induced lymphocyte proliferation assays, which indicates that a single anti-HLA (human leukocyte antigen) class II antibody is effective in blocking the biological effects of these toxins. These results demonstrate the possibility of using anti-HLA class II antibodies in a clinical setting as an antagonist to staphylococcal enterotoxinmediated pathogenesis.
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PMID:Inhibition of staphylococcal enterotoxin-driven lymphocyte proliferation by anti-MHC class II monoclonal antibody. 857 91


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