V<sub>β</sub>‐restricted T cell adherence to endothelial cells: A mechanism for superantigen‐dependent vascular injury

Brogan, Paul A.; Shah, Vanita; Klein, Nigel; Dillon, Michael J.

doi:10.1002/art.20021

Cited by 44 publications

(39 citation statements)

References 35 publications

(42 reference statements)

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“…Although best known for its capacity to produce symptoms of food poisoning upon ingestion, it is an important mediator of nonmenstrual toxic shock syndrome upon entry to the general circulation and systemic tissues (Schlievert, 1986;Wright and Trott, 1988). SEB is also capable of enhancing specific humoral immunity (Torres et al, 2002) and of exacerbating autoimmune diseases such as experimental allergic encephalomyelitis (Schiffenbauer et al, 1993) and Kawasaki disease (Brogan et al, 2004). Its stability, potency to incapacitate, and ability to be delivered in aerosol form led SEB to be developed as a biological warfare agent in the 1960s, and it is listed by the U.S. Centers for Disease Control among Class B (second highest priority) agents that pose a bioterrorism threat.…”

Section: Relationship To Previous Studiesmentioning

confidence: 99%

CNS activational responses to staphylococcal enterotoxin B: T-lymphocyte-dependent immune challenge effects on stress-related circuitry

Serrats

Sawchenko

2006

J. Comp. Neurol.

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Staphylococcal enterotoxin B (SEB) is a bacterial superantigen that engages the immune system in a T-lymphocyte-dependent manner and induces a cytokine profile distinct from that elicited by the better-studied bacterial pathogen analog, lipopolysaccharide (LPS). Because of reports of SEB recruiting central nervous system (CNS) host defense mechanisms via pathways in common with LPS, we sought to further characterize central systems impacted by this agent. Rats were treated with SEB at doses of 50-5,000 mug/kg, and killed 0.5-6 hours thereafter. SEB injection produced a discrete pattern of Fos induction in brain that peaked at 2-3 hours postinjection and whose strength was dose-related. Induced Fos expression was predominantly subcortical and focused in a set of interconnected central autonomic structures, including aspects of the bed n. of the stria terminalis, central amygdala and lateral parabrachial nuclei; functionally related (and LPS-responsive) cell groups in the n. solitary tract, ventrolateral medulla, and paraventricular hypothalamic n. (PVH) were, by contrast, weakly responsive. SEB also activated cell groups in the limbic forebrain (lateral septal n, medial prefrontal cortex) and hypothalamic GABAergic neurons, which could account for its failure to elicit reliable increases in Fos-ir or corticotropin-releasing factor (CRF) mRNA in the PVH. SEB nevertheless did provoke reliable pituitary-adrenal secretory responses. The identification of subsets of central autonomic and limbic forebrain structures that are sensitive to SEB provides a basis for a systems-level understanding of the physiological and behavioral effects attributed to the superantigen. Core SEB-responsive cell groups exclude a medullary-PVH circuit implicated in pituitary-adrenal responses to LPS.

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Section: Relationship To Previous Studiesmentioning

confidence: 99%

CNS activational responses to staphylococcal enterotoxin B: T-lymphocyte-dependent immune challenge effects on stress-related circuitry

Serrats

Sawchenko

2006

J. Comp. Neurol.

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“…In addition, a dose-response curve for NMP generation from primed neutrophils stimulated with chimeric IgG3 PR3-ANCA was plotted over the concentration 0-20 mg/ml ( Figure 2C). Supernatants from experiments were obtained by centrifugation at 5000 3 g for 5 minutes to remove cells and large debris, as previously described, 47 and frozen for future analysis using flow cytometry (see later). A single freeze-thaw cycle did not alter the number, phenotype, or activity of the NMPs (data not shown).…”

Section: Generation Of Nmps From Neutrophils Using Ancasmentioning

confidence: 99%

“…47 To investigate the contribution of oxidative stress to endothelial activation, HUVECs were pretreated with the antioxidants 3 mM MnTBPA or 100 mM of the NADPH oxidase inhibitor apocynin for 30 minutes before NMP exposure. To exclude any possibility of lowgrade endothelial activation derived from TNF-a contamination (used in the neutrophil-priming step prior to stimulation with ANCAs), infliximab (Remicade; Schering-Plough), a chimeric monoclonal anti-TNF-a antibody, at a concentration of 10 mg/ml equivalent to therapeutic plasma concentrations used in clinical practice 49 was added before NMP exposure in some experiments.…”

Section: Assessment Of Endothelial Cell Activationmentioning

confidence: 99%

Anti-Neutrophil Cytoplasmic Antibodies Stimulate Release of Neutrophil Microparticles

Hong

Eleftheriou

Hussain

et al. 2012

Journal of the American Society of Nephrology

138

151

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The mechanisms by which anti-neutrophil cytoplasmic antibodies (ANCAs) may contribute to the pathogenesis of ANCA-associated vasculitis are not well understood. In this study, both polyclonal ANCAs isolated from patients and chimeric proteinase 3-ANCA induced the release of neutrophil microparticles from primed neutrophils. These microparticles expressed a variety of markers, including the ANCA autoantigens proteinase 3 and myeloperoxidase. They bound endothelial cells via a CD18-mediated mechanism and induced an increase in endothelial intercellular adhesion molecule-1 expression, production of endothelial reactive oxygen species, and release of endothelial IL-6 and IL-8. Removal of the neutrophil microparticles by filtration or inhibition of reactive oxygen species production with antioxidants abolished microparticle-mediated endothelial activation. In addition, these microparticles promoted the generation of thrombin. In vivo, we detected more neutrophil microparticles in the plasma of children with ANCAassociated vasculitis compared with that in healthy controls or those with inactive vasculitis. Taken together, these results support a role for neutrophil microparticles in the pathogenesis of ANCA-associated vasculitis, potentially providing a target for future therapeutics.

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“…T cells migrate from the peripheral circulation to become activated directly on the surface of endothelium and then move to the perivascular compartment of lesional tissue of KD patients. 86 Although Vb skewing has been shown in peripheral blood of some KD patients, this has not been a consistent finding. Tissue sequestration of Vb-restricted T cells might explain the low numbers of Vb-restricted T cells in peripheral blood of some acute KD patients.…”

Section: Toxic Shock Syndromeerelated Syndromesmentioning

confidence: 96%

Superantigens in dermatology

Macias

Pereira

Rietkerk

et al. 2011

Journal of the American Academy of Dermatology

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V_β‐restricted T cell adherence to endothelial cells: A mechanism for superantigen‐dependent vascular injury

Cited by 44 publications

References 35 publications

CNS activational responses to staphylococcal enterotoxin B: T-lymphocyte-dependent immune challenge effects on stress-related circuitry

CNS activational responses to staphylococcal enterotoxin B: T-lymphocyte-dependent immune challenge effects on stress-related circuitry

Anti-Neutrophil Cytoplasmic Antibodies Stimulate Release of Neutrophil Microparticles

Superantigens in dermatology

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Vβ‐restricted T cell adherence to endothelial cells: A mechanism for superantigen‐dependent vascular injury

Cited by 44 publications

References 35 publications

CNS activational responses to staphylococcal enterotoxin B: T-lymphocyte-dependent immune challenge effects on stress-related circuitry

CNS activational responses to staphylococcal enterotoxin B: T-lymphocyte-dependent immune challenge effects on stress-related circuitry

Anti-Neutrophil Cytoplasmic Antibodies Stimulate Release of Neutrophil Microparticles

Superantigens in dermatology

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Product

Resources

About

V_β‐restricted T cell adherence to endothelial cells: A mechanism for superantigen‐dependent vascular injury