Clearance of Staphylococcus aureus nasal carriage is T cell dependent and mediated through interleukin-17A expression and neutrophil influx - Wikidata - awgldk - TriplyDB

Clearance of Staphylococcus aureus nasal carriage is T cell dependent and mediated through interleukin-17A expression and neutrophil influx

Clearance of Staphylococcus aureus nasal carriage is T cell dependent and mediated through interleukin-17A expression and neutrophil influx

http://www.wikidata.org/entity/Q36911421

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Mechanisms of Bacterial Colonization of the Respiratory Tract An innate antiviral pathway acting before interferons at epithelial surfaces.Staphylococcus aureus - antimicrobial resistance and the immunocompromised child.Staphylococcus aureus Infections After Elective Cardiothoracic Surgery: Observations From an International Randomized Placebo-Controlled Trial of an Investigational S aureus Vaccine The role of the local microbial ecosystem in respiratory health and disease.A Multiple Antigenic Peptide Mimicking Peptidoglycan Induced T Cell Responses to Protect Mice from Systemic Infection with Staphylococcus aureus.Genome-wide association study reveals a locus for nasal carriage of Staphylococcus aureus in Danish crossbred pigs.High Frequency and Diversity of Antimicrobial Activities Produced by Nasal Staphylococcus Strains against Bacterial Competitors Antigen delivery to dendritic cells shapes human CD4+ and CD8+ T cell memory responses to Staphylococcus aureus Importance of B Lymphocytes and the IgG-Binding Protein Sbi in Staphylococcus aureus Skin Infection.The T Cell Response to Staphylococcus aureus Host innate inflammatory factors and staphylococcal protein A influence the duration of human Staphylococcus aureus nasal carriage.Leishmania amazonensis amastigotes trigger neutrophil activation but resist neutrophil microbicidal mechanisms.Interleukin-17A (IL-17A) and IL-17F Are Critical for Antimicrobial Peptide Production and Clearance of Staphylococcus aureus Nasal Colonization.Fungal morphogenetic pathways are required for the hallmark inflammatory response during Candida albicans vaginitis.Omics Approaches for the Study of Adaptive Immunity to Staphylococcus aureus and the Selection of Vaccine Candidates.Myeloid-derived suppressor cells contribute to Staphylococcus aureus orthopedic biofilm infection.Staphylococcal vaccine development: review of past failures and plea for a future evaluation of vaccine efficacy not only on staphylococcal infections but also on mucosal carriage.Staphylococcus aureus Colonization: Modulation of Host Immune Response and Impact on Human Vaccine Design.Staphylococcal bicomponent pore-forming toxins: targets for prophylaxis and immunotherapy.Phagocyte subsets and lymphocyte clonal deletion behind ineffective immune response to Staphylococcus aureus.Permissive and protective roles for neutrophils in leishmaniasis.Nasopharyngeal colonization with Streptococcus pneumoniae triggers dendritic cell dependent antibody responses against invasive disease in mice.Staphylococcus aureus Colonization Modulates Tic Expression and the Host Immune Response in a Girl with Tourette Syndrome.Inhibition of fracture healing in the presence of contamination by Staphylococcus aureus: Effects of growth state and immune response.Cholinergic PET imaging in infections and inflammation using 11C-donepezil and 18F-FEOBV.Ratio of T-Helper Type 1 (Th1) to Th17 Cytokines in Whole Blood Is Associated With Human β-Defensin 3 Expression in Skin and Persistent Staphylococcus aureus Nasal Carriage.Secondary Bacterial Infections Associated with Influenza Pandemics Combining Two Methods of Global Sensitivity Analysis to Investigate MRSA Nasal Carriage Model.Staphylococcus aureus and Influenza A Virus: Partners in Coinfection.Staphylococcus aureus: the current state of disease, pathophysiology and strategies for prevention.Mathematical Model for MRSA Nasal Carriage.Mortality among recipients of the Merck V710 Staphylococcus aureus vaccine after postoperative S. aureus infections: an analysis of possible contributing host factors.Involvement of the IL-23/IL-17 axis and the Th17/Treg balance in the pathogenesis and control of autoimmune arthritis.Secretion of IL-16 through TNFR1 and calpain-caspase signaling contributes to MRSA pneumonia.Development of persistent gastrointestinal S. aureus carriage in mice.Lipid moieties on lipoproteins of commensal and non-commensal staphylococci induce differential immune responses.S. aureus colonization induces strain-specific suppression of IL-17.A D-Alanine Auxotrophic Live Vaccine is Effective against Lethal Infection Caused by Staphylococcus aureus.Distinct T-helper cell responses to Staphylococcus aureus bacteremia reflect immunologic comorbidities and correlate with mortality.

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P2860

Clearance of Staphylococcus aureus nasal carriage is T cell dependent and mediated through interleukin-17A expression and neutrophil influx

http://www.wikidata.org/entity/Q36911421

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2013 nî lūn-bûn

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Infection and Immunity

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Clearance of Staphylococcus au ...... pression and neutrophil influx

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Janette M Harro

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Mark E Shirtliff

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Nathan K Archer

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P2860

Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12

STAT3 mutations in the hyper-IgE syndrome

IL-17A-producing neutrophil-regulatory Tn lymphocytes

Staphylococcus epidermidis Esp inhibits Staphylococcus aureus biofilm formation and nasal colonization

TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells

Coagulase and protein A polymorphisms do not contribute to persistence of nasal colonisation by Staphylococcus aureus.

National Nosocomial Infections Surveillance (NNIS) System Report, Data Summary from January 1990-May 1999, issued June 1999. A report from the NNIS System.

Nasal carriage as a source of Staphylococcus aureus bacteremia. Study Group.

Regulating human Th17 cells via differential expression of IL-1 receptor.

IL-17 is essential for host defense against cutaneous Staphylococcus aureus infection in mice

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2070-2075

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10.1128/IAI.00084-13

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81

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3676016

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