Selective expansion of T cells expressing V beta 2 in toxic shock syndrome.

Choi, Yongwon; Lafferty, Joyce; Clements, Janice; Todd, James K.; Gelfand, Erwin W.; Kappler, John W.; Marrack, Philippa; Kotzin, Brian L.

doi:10.1084/jem.172.3.981

Cited by 343 publications

(197 citation statements)

References 18 publications

(34 reference statements)

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“…The only exception to this appears to be TSST-1. TSST-1 binds to V␤2.1 TCRs and causes unambiguous elevation of TCRBV2S1 mRNA levels (28,29,31). It has no effect on TCRBV17S1 transcription (data not shown), but does cause a small but significant elevation of TCRBV3S1 transcription in all subjects tested.…”

Section: Discussionmentioning

confidence: 94%

Antigen Triggering Selectively Increases TCRBV Gene Transcription

Lennon

Sillibourne

Furrie

et al. 2000

The Journal of Immunology

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When the TCR binds Ag it is phosphorylated, internalized, and degraded. We wished to examine whether this process was accompanied by a specific concomitant increase in TCR mRNA levels. To do this, PBMC and a T cell clone were cultured with a series of superantigens and an alloantigen. Only T cells specifically responding to an antigenic stimulus had increased levels of TCR β-chain variable (TCRBV)-specific mRNA. This response was apparent after 48 h, peaked around 72 h, and was still elevated after 7 days. Increased gene transcription appeared to be driven solely by Ag as specific Ag depletion prevented culture supernatants transferring this effect. The level of TCRBV mRNA elevation was not influenced by the stimulating Ag, but appeared dependent on the gene encoding the stimulated TCR. Reporter gene assays, using cloned TCRBV gene promoters, confirmed both that TCR gene transcription rises after stimulation and that basal and stimulated levels of TCR transcription vary between different TCRBV genes. These data conclusively demonstrate that there is no direct relationship between TCRBV mRNA and T cell number, and that future repertoire studies must take both factors into account.

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Section: Discussionmentioning

confidence: 94%

Antigen Triggering Selectively Increases TCRBV Gene Transcription

Lennon

Sillibourne

Furrie

et al. 2000

The Journal of Immunology

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“…Sensitivity differences of mice strains to bacterial superantigens were probably related to the type of MHC class II found on antigen-presenting cells and Vβ populations among T cells (Choi et al, 1990). The mean value of the TSST-1 LD-50 obtained for BALB/c mice was 2.38 times lower than that of Stiles et al (1995) (47.2µg/kg -0.94µg/mouse, 95% confidence limit of 15.2 -200µg/kg), but the confidence limits of both studies greatly overlap.…”

Section: Resultsmentioning

confidence: 99%

The use of mice as animal model for testing acute toxicity (LD-50) of toxic shock syndrome toxin

Dias

Carmo

Heneine

et al. 2009

Arq. Bras. Med. Vet. Zootec.

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Acute toxicity test (LD-50) using toxic shock syndrome toxin (TSST-1) was tested in BALB/c, C57BL/6 and Swiss mice. Animals (n = 10) were intraperitoneally injected with TSST-1 (0.01-10.0µg/mouse) followed 4h later by potentiating dose of lipopolysaccharide (75.0µg of LPS -E. coli O111:B4) and cumulative mortality was recorded over 72h. Control animals received either TSST-1 or LPS alone. The data were submitted to quiSquare test and acute toxicity test was calculated by probit analysis (confidence limits expressed as µg toxin/kg). BALB/c mice was the most sensitive (20.0µg/kg, 95% confidence limits: 9.0-92.0) followed by C57BL/6 (38.5µg/kg, 95% confidence limits: 9.11-401.6). Data from Swiss mice was not conclusive, indicating only low sensitivity. Selection of the animal model and standardization of the experiment are fundamental for the development of serum neutralization tests used for final quality control of vaccine production.Keywords: mice, TSST-1, acute toxicity (LD-50), Staphylococcus 0), seguida da C57BL/6 (38,6 RESUMO A toxicidade aguda (DL-50) da toxina da síndrome do choque tóxico (TSST-1) foi testada em linhagens de camundongos BALB/c, C57BL/6 e Suíça. Os animais (n=10) inoculados intraperitoneal com doses crescentes de toxina (0,01 -10,0µg/animal) receberam 4h após 75µg de LPS (E. coli O111: B4). A toxicidade aguda (DL-50) foi observada por um período de 72h e os dados submetidos ao teste de qui-quadrado. Os resultados e os limites de confiança foram expressos em µg de toxina/kg. A linhagem BALB/c apresentou maior sensibilidade

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“…As superantigens these proteins bind to MHC class II molecules and activate a large set ofT cells in a V/3-specific fashion (6)(7)(8)(9)(10)(11)(12). This T cell stimulation and the accompanying massive release of lymphokines appear to play an essential role in the toxicity of these proteins (13,14).…”

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confidence: 99%

Monoclonal antibodies defining functional sites on the toxin superantigen staphylococcal enterotoxin B.

Hamad

Herman

Marrack

et al. 1994

The Journal of Experimental Medicine

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SummaryFour monoclonal antibodies (mAbs) were produced binding to four nonoverlapping epitopes on the superantigen staphylococcal enterotoxin B (SEB). The mAbs were tested for their ability to detect SEB bound to major histocompatibility complex (MHC) class II, to inhibit SEB binding to MHC class II, to inhibit SEB stimulation of T cell hybridomas, to bind to various nonfunctional mutants of SEB, and to capture and present SEB and its mutants to T cells in the absence of MHC class II. We concluded that two mAbs, B344 and B327, bound to epitopes not required for superantigen function, one mAb, 2B33, blocked an MHC interaction site on SEB, and the fourth mAb, B87, blocked the T cell recognition site on SEB. Moreover, two mAbs (B344 and 2B33) were capable of presenting SEB, although much less efficiently than APC, to CD4-but not CD4 § T cell hybridomas. The results confirm the functional domains on SEB originally defined by mutation and show that MHC class II is not always an essential component of the superantigen ligand.S taphylococcus aureus produces a set of exotoxin superantigens that cause food poisoning and toxic shock in man and rapid weight loss in mice sometimes leading to death (1-5). As superantigens these proteins bind to MHC class II molecules and activate a large set ofT cells in a V/3-specific fashion (6-12). This T cell stimulation and the accompanying massive release of lymphokines appear to play an essential role in the toxicity of these proteins (13,14).Although the amino acid sequences of the staphylococcal toxins are related, each has a unique V~ specificity. For example, in mice staphylococcal enterotoxin B (SEB) 1 stimulates T cells bearing V~7, 8.1, 8.2, and 8.3 (6, 10, 11), whereas SEA stimulates T cells bearing V/31, 3, 11, and 17a (10). We have identified mutants of SEB impaired either for binding to MHC or for interaction with ol/3 TCR-VBs (14). These mutations in SEB also eliminated in vivo toxicity in mice. When mapped on the structure of SEB, these mutations indicated different sites on the SEB surface for orb TCR versus MHC interaction (15).In the current study we have confirmed these conclusions using a set of four anti-SEB mAbs specific for four nonoveri Abbreviations used in this paper: CTM, complete tissue culture medium; FBS, fetal bovine serum; SEB, staphylococcal enterotoxin B; F-SEB, fluoresceinated SEB. lapping epitopes on SEB. Two of these antibodies define an MHC and an c~/3 TCR-interaction site on SEB, whereas, the other two react with sites not involved in SEB superantigen activity. Moreover, we found that two of these mAbs could substitute for MHC class II in presentation of SEB to T cell hybridomas. Materials and MethodsCell Lines. Three T cell hybridomas were used in these studies, all derived from B10.BR mice. KS-6.1 (VB8.2+) and

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Selective expansion of T cells expressing V beta 2 in toxic shock syndrome.

Cited by 343 publications

References 18 publications

Antigen Triggering Selectively Increases TCRBV Gene Transcription

Antigen Triggering Selectively Increases TCRBV Gene Transcription

The use of mice as animal model for testing acute toxicity (LD-50) of toxic shock syndrome toxin

Monoclonal antibodies defining functional sites on the toxin superantigen staphylococcal enterotoxin B.

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