Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection. - Wikidata - wikimedia - TriplyDB

Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.

Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.

http://www.wikidata.org/entity/Q36911822

about

Interleukin-22 ameliorates acute severe pancreatitis-associated lung injury in mice Influenza and Bacterial Superinfection: Illuminating the Immunologic Mechanisms of Disease The crystal structure of zebrafish IL-22 reveals an evolutionary, conserved structure highly similar to that of human IL-22 The immunology of influenza virus-associated bacterial pneumonia Influenza vaccines to control influenza-associated bacterial infection: where do we stand?Why is coinfection with influenza virus and bacteria so difficult to control?Multiplex Analysis of Serum Cytokines in Humans with Hantavirus Pulmonary Syndrome.Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense.Interleukin-34 inhibits hepatitis B virus replication in vitro and in vivo.The oral commensal Streptococcus mitis shows a mixed memory Th cell signature that is similar to and cross-reactive with Streptococcus pneumoniae.PACAP38 differentially effects genes and CRMP2 protein expression in ischemic core and penumbra regions of permanent middle cerebral artery occlusion model mice brain.Tailored immune responses: novel effector helper T cell subsets in protective immunity.Interleukin-22: immunobiology and pathology.Emerging Role of Interleukin 22 in Hepatitis B Virus Infection: a Double-edged Sword.Lambda Interferon Restructures the Nasal Microbiome and Increases Susceptibility to Staphylococcus aureus Superinfection A pro-inflammatory role for Th22 cells in Helicobacter pylori-associated gastritis.A Toll-Like Receptor 5 Agonist Improves the Efficacy of Antibiotics in Treatment of Primary and Influenza Virus-Associated Pneumococcal Mouse Infections.TRAIL+ monocytes and monocyte-related cells cause lung damage and thereby increase susceptibility to influenza-Streptococcus pneumoniae coinfection.Epithelial-intrinsic IKKα expression regulates group 3 innate lymphoid cell responses and antibacterial immunity.IL-22 Defect During Streptococcus pneumoniae Infection Triggers Exacerbation of Chronic Obstructive Pulmonary Disease Attenuated Airway Epithelial Cell Interleukin-22R1 Expression in the Infant Nonhuman Primate Lung.MicroRNA-155 regulates host immune response to postviral bacterial pneumonia via IL-23/IL-17 pathway.The Role of IL-22 in Viral Infections: Paradigms and Paradoxes Toll-like receptor 2-dependent protection against pneumococcal carriage by immunization with lipidated pneumococcal proteins.Conventional NK cells can produce IL-22 and promote host defense in Klebsiella pneumoniae pneumonia.Immune dysfunction and bacterial coinfections following influenza.Role of type 1 natural killer T cells in pulmonary immunity.Dysregulation in lung immunity - the protective and pathologic Th17 response in infection.A tale of two cytokines: IL-17 and IL-22 in asthma and infection.Therapeutic opportunities of the IL-22-IL-22R1 system.Immunomodulators targeting MARCO expression improve resistance to postinfluenza bacterial pneumonia.The inflammatory response triggered by Influenza virus: a two edged sword.Lung-resident γδ T cells and their roles in lung diseases.IL-17 in the lung: The Good, the Bad, and the Ugly.Influenza Casts a Lung Shadow.IL-22 exacerbates weight loss in a murine model of chronic pulmonary Pseudomonas aeruginosa infection Influenza A virus-induced release of interleukin-10 inhibits the anti-microbial activities of invariant natural killer T cells during invasive pneumococcal superinfection.Interleukin-22 protects against non-typeable Haemophilus influenzae infection: alteration during chronic obstructive pulmonary disease.Examining the Effects of External or Internal Radiation Exposure of Juvenile Mice on Late Morbidity after Infection with Influenza A.Innate Lymphoid Cells Are the Predominant Source of IL-17A during the Early Pathogenesis of Acute Respiratory Distress Syndrome.

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Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.

http://www.wikidata.org/entity/Q36911822

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Interleukin-22 reduces lung in ...... secondary bacterial infection.

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Adeline Barthelemy

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Carl De Trez

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Elodie Macho Fernandez

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Fany Blanc

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François Trottein

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Joelle Renneson

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Josette Fontaine

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Laure Dumoutier

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Michel-René Huerre

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Pierre Gosset

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P2860

The pathology of influenza virus infections

Human interleukin-10-related T cell-derived inducible factor: molecular cloning and functional characterization as an hepatocyte-stimulating factor

Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides

Interleukin-22 drives endogenous thymic regeneration in mice

Pathological versus protective functions of IL-22 in airway inflammation are regulated by IL-17A

Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness

Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling

IL-22 increases the innate immunity of tissues

IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine

Innate Stat3-mediated induction of the antimicrobial protein Reg3γ is required for host defense against MRSA pneumonia

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6911-6924

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10.1128/JVI.02943-12

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12

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87

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Jean-Christophe Renauld

Mustapha Si-Tahar

Laurye Van Maele

Christophe Paget

Christelle Faveeuw

Jean-Claude Sirard

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2013-04-17T00:00:00Z

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23596287

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3676141

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