T-cell Activation and Proliferation in a Case of Recurrent Menstrual Toxic Shock Syndrome

1996 ◽  
Vol 284 (2-3) ◽  
pp. 164-169 ◽  
Author(s):  
Mardjan Arvand ◽  
Helmut Hahn
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Toxic Shock Syndrome ◽  
Cell Activation ◽  
Toxic Shock

scholarly journals Protection against lethal toxic shock by targeted disruption of the CD28 gene.

1996 ◽  
Vol 183 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
B Saha ◽  
D M Harlan ◽  
K P Lee ◽  
C H June ◽  
R Abe
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Toxic Shock Syndrome ◽  
Cell Activation ◽  
Dose Effect ◽  
Tnf Alpha ◽  
Toxic Shock ◽  
Costimulatory Signals ◽  
Toxigenic Strains

Toxic shock syndrome (TSS) is a multi system disorder resulting from superantigen-mediated cytokine production. Nearly 90% of the clinical cases of TSS arise due to an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by toxigenic strains of Staphylococcus aureus. It is clearly established that besides antigen-specific signals a variety of costimulatory signals are required for full T cell activation. However, the nature and potential redundancy of costimulatory signals are incompletely understood, particularly with regards to superantigen-mediated T cell activation in vivo. Here we report that CD28-deficient mice (CD28-/-) are completely resistant to TSST-1-induced lethal TSS while CD28 (+/-) littermate mice were partially resistant to TSST-1. The mechanism for the resistance of the CD28 (-/-) mice was a complete abrogation of TNF-alpha accumulation in the serum and a nearly complete (90%) impairment of IFN-gamma secretion in response to TSST-1 injection. In contrast, the serum level of IL-2 was only moderately influenced by the variation of CD28 expression. CD28 (-/-) mice retained sensitivity to TNF-alpha as demonstrated by equivalent lethality after cytokine injection. These findings establish an essential requirement for CD28 costimulatory signals in TSST-1-induced TSS. The hierarchy of TSST-1 resistance among CD28 wild-type (CD28+/+), CD28 heterozygous (CD28+/-), and CD28-/- mice suggests a gene-dose effect, implying that the levels of T cell surface CD28 expression critically regulate superantigen-mediated costimulation. Finally, as these results demonstrate the primary and non-redundant role of CD28 receptors in the initiation of the in vivo cytokine cascade, they suggest therapeutic approaches for superantigen-mediated immunopathology.

Toll-like receptor 2 ligands on the staphylococcal cell wall downregulate superantigen-induced T cell activation and prevent toxic shock syndrome

2009 ◽  
Vol 15 (6) ◽  
pp. 641-648 ◽  
Author(s):  
Thu A Chau ◽  
Michelle L McCully ◽  
William Brintnell ◽  
Gary An ◽  
Katherine J Kasper ◽  
...  
Keyword(s):  
Cell Wall ◽  
T Cell ◽  
T Cell Activation ◽  
Toxic Shock Syndrome ◽  
Cell Activation ◽  
Toll Like Receptor ◽  
Toxic Shock ◽  
Toll Like Receptor 2

scholarly journals Superantigenic TCR Vbeta 21.3 signature in Multisystem Inflammatory Syndrome in Children

2021 ◽  
Author(s):  
Marion Moreews ◽  
Kenz Le Gouge ◽  
Alicia Bellomo ◽  
Christophe Malcus ◽  
Rémi Pescarmona ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Kawasaki Disease ◽  
T Cell Activation ◽  
Toxic Shock Syndrome ◽  
Healthy Children ◽  
Toxic Shock ◽  
Hla Dr ◽  
Inflammatory Syndrome

AbstractObjectivesMultiple Inflammatory Syndrome in Children (MIS-C) is the most severe pediatric form of COVID-19 and occurs in previously healthy children. MIS-C combines features of Kawasaki disease and Toxic Shock Syndrome (TSS).MethodsChildren with suspected MIS-C were included within the first week of diagnosis and a large scale immunoassay was performed to determein the immunologic signature of these patients.ResultsWe characterized the immunological profile of 27 MIS-C cases in comparison with 4 KD and 4 TSS cases. Similarly to TSS, an increase of serum inflammatory cytokines (IL-6, TNF-a, CD25s) was observed in MIS-C contrasting with low expression of HLA-DR monocytes, a feature often associated with immune paralysis. Expansions of T cells expressing the Vβ21.3 T cell receptor β chain variable region were detected in both CD4 and CD8 subsets in almost 50% of patients and Vβ21.3-positive T cells expressed high level of HLA-DR highlighting their specific activation. TCR sequencing uncovered the polyclonal nature of the Vβ 21.3+ population. SARS-CoV2 antigene-specific production of interferon gamma in T cells was not increased in MIS-C T cells compared to COVID-19 patients suggesting the antigen-specific immune response in MIS-C patients is not pivotal to the manifestation.ConclusionsOur findings argue in favor of a strong activation of the immune system related to a superantigenic immune response in MIS-C with a specific polyclonal Vβ21.3 T cell expansion.Key messagesWhat is already known about this subject ?MIS-C occurs 3-5 weeks after acute SARS-CoV2 infection and overlap features of Toxic Shock syndrome and Kawasaki disease.MIS-C appears different in term of cytokine and autoantibodies generation from KD with subtle signs of T cells activationWhat does this study add?This study demonstrates that Vβ21.3+ CD4 and CD8 T cells are highly increased in about 50% of MIS-C and distinctive of the Vβ2+ expansion observed in toxic shock syndrome in This reflects a specific T cell activation and cytokine release syndrome similar to toxic shock syndromeHow mich this impact on clinical practice or future developments?Vβ21.3+ signature can be available on a short term basis by flowcytometry and represents a signature of the MIS-C.As for TSS, immunomodulating therapies may revert the superantigenic activation and resolve this life threatening pediatric condition.

scholarly journals High Titer Persistent Neutralizing Antibodies Induced by TSST-1 Variant Vaccine Against Toxic Shock Cytokine Storm

Toxins ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 640
Author(s):  
Andreas Roetzer ◽  
Norbert Stich ◽  
Nina Model ◽  
Michael Schwameis ◽  
Christa Firbas ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Neutralizing Antibodies ◽  
Cell Activation ◽  
High Titer ◽  
Neutralizing Antibody ◽  
Cytokine Storm ◽  
Toxic Shock ◽  
Antibody Titers ◽  
Toxic Shock Syndrome Toxin

Staphylococcal superantigen toxins lead to a devastating cytokine storm resulting in shock and multi-organ failure. We have previously assessed the safety and immunogenicity of a recombinant toxic shock syndrome toxin 1 variant vaccine (rTSST-1v) in clinical trials (NCT02971670 and NCT02340338). The current study assessed neutralizing antibody titers after repeated vaccination with escalating doses of rTSST-1v. At study entry, 23 out of 34 subjects (67.6%) had neutralizing antibody titers inhibiting T cell activation as determined by 3H-thymidine incorporation at a serum dilution of ≤1:100 with similar figures for inhibition of IL-2 activation (19 of 34 subjects, 55.9%) as assessed by quantitative PCR. After the first vaccination, numbers of subjects with neutralization titers inhibiting T cell activation (61.7% ≥ 1:1000) and inhibiting IL-2 gene induction (88.2% ≥ 1:1000) increased. The immune response was augmented after the second vaccination (inhibiting T cell activation: 78.8% ≥ 1:1000; inhibiting IL-2 induction: 93.9% ≥ 1:1000) corroborated with a third immunization months later in a small subgroup of subjects. Assessment of IFNγ, TNFα and IL-6 inhibition revealed similar results, whereas neutralization titers did not change in placebo participants. Antibody titer studies show that vaccination with rTSST-1v in subjects with no/low neutralizing antibodies can rapidly induce high titer neutralizing antibodies persisting over months.

scholarly journals Involvement of Enterotoxins G and I in Staphylococcal Toxic Shock Syndrome and Staphylococcal Scarlet Fever

1999 ◽  
Vol 37 (8) ◽  
pp. 2446-2449 ◽  
Author(s):  
Sophie Jarraud ◽  
Grégoire Cozon ◽  
François Vandenesch ◽  
Michèle Bes ◽  
Jerome Etienne ◽  
...  
Keyword(s):  
T Cell Activation ◽  
Scarlet Fever ◽  
Toxic Shock Syndrome ◽  
Cell Activation ◽  
Target Genes ◽  
Pcr Amplification ◽  
Toxic Shock ◽  
Specific Flow ◽  
Staphylococcal Enterotoxins ◽  
Staphylococcal Toxic Shock Syndrome

We investigated the involvement of the recently described staphylococcal enterotoxins G and I in toxic shock syndrome. We reexamined Staphylococcus aureus strains isolated from patients with menstrual and nonmenstrual toxic shock syndrome (nine cases) or staphylococcal scarlet fever (three cases). These strains were selected because they produced none of the toxins known to be involved in these syndromes (toxic shock syndrome toxin 1 and enterotoxins A, B, C, and D), enterotoxin E or H, or exfoliative toxin A or B, despite the fact that superantigenic toxins were detected in a CD69-specific flow cytometry assay measuring T-cell activation. Sets of primers specific to the enterotoxin G and I genes (seg andsei, respectively) were designed and used for PCR amplification. All of the strains were positive for seg andsei. Sequence analysis confirmed that the PCR products, corresponded to the target genes. We suggest that staphylococcal enterotoxins G and I may be capable of causing human staphylococcal toxic shock syndrome and staphylococcal scarlet fever.

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

1990 ◽  
Vol 172 (3) ◽  
pp. 981-984 ◽  
Author(s):  
Y Choi ◽  
J A Lafferty ◽  
J R Clements ◽  
J K Todd ◽  
E W Gelfand ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Toxic Shock Syndrome ◽  
Large Fraction ◽  
Gene Segment ◽  
Disease Process ◽  
Toxic Shock ◽  
Human T Cell ◽  
Beta 2

Infection with Staphylococcus aureus and the production of toxic shock syndrome toxin-1 (TSST-1) have been implicated in the pathogenesis of toxic shock syndrome. Previous in vitro studies have demonstrated that TSST-1 is a powerful but selective stimulator of human T cells, and that the majority of activated cells express the TCR V beta 2 gene segment. We therefore studied patients with toxic shock syndrome using a modification of the PCR to determine if expansion of V beta 2+ T cells is a marker of the in vivo disease process. Five of eight patients studied demonstrated markedly elevated levels of circulating V beta 2+ T cells, whereas none showed significantly elevated levels of T cells expressing other V beta gene segments. The results suggest that toxin-mediated T cell activation, which involves a large fraction of the human T cell repertoire, may be critical in the pathogenesis of this disease.

T cell activation and cytokine release in streptococcal toxic shock-like syndrome

1993 ◽  
Vol 122 (5) ◽  
pp. 727-729 ◽  
Author(s):  
David Nadal ◽  
Roger P. Lauener ◽  
Christian P. Braegger ◽  
Achim Kaufhold ◽  
Burkhard Simma ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cytokine Release ◽  
Toxic Shock
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