Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection. - Wikidata - awgldk - TriplyDB

Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection.

Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection.

http://www.wikidata.org/entity/Q45733086

about

Influenza virus antigenic variation, host antibody production and new approach to control epidemics Systemic delivery of oncolytic viruses: hopes and hurdles Natural antibody and complement mediate neutralization of influenza virus in the absence of prior immunity Complement contributes to inflammatory tissue destruction in a mouse model of Ross River virus-induced disease An AGM model for changes in complement during pregnancy: neutralization of influenza virus by serum is diminished in late third trimester Modeling host genetic regulation of influenza pathogenesis in the collaborative cross Complement activation is required for induction of a protective antibody response against West Nile virus infection West Nile virus nonstructural protein NS1 inhibits complement activation by binding the regulatory protein factor H Protective immune responses against West Nile virus are primed by distinct complement activation pathways Innate immunity to influenza virus: implications for future therapy Complement and its role in protection and pathogenesis of flavivirus infections Evasion of innate and adaptive immunity by flaviviruses Infections of People with Complement Deficiencies and Patients Who Have Undergone Splenectomy Complement: a key system for immune surveillance and homeostasis Innate and adaptive immunologic functions of complement in the host response to Listeria monocytogenes infection.Age at Vaccination and Timing of Infection Do Not Alter Vaccine-Associated Enhanced Respiratory Disease in Influenza A Virus-Infected Pigs.Genomic profiling of tumor necrosis factor alpha (TNF-alpha) receptor and interleukin-1 receptor knockout mice reveals a link between TNF-alpha signaling and increased severity of 1918 pandemic influenza virus infection.Synergy between the classical and alternative pathways of complement is essential for conferring effective protection against the pandemic influenza A(H1N1) 2009 virus infection.A protective role for complement C3 protein during pandemic 2009 H1N1 and H5N1 influenza A virus infection The innate immunity of guinea pigs against highly pathogenic avian influenza virus infection Viral infection of the lung: host response and sequelae Complement C5 activation during influenza A infection in mice contributes to neutrophil recruitment and lung injury.Surviving mousepox infection requires the complement system C3d regulates immune checkpoint blockade and enhances antitumor immunity.Complement as an endogenous adjuvant for dendritic cell-mediated induction of retrovirus-specific CTLs.Role and mechanism of action of complement in regulating T cell immunity.Complement and viral pathogenesis Immunogenicity to biologics: mechanisms, prediction and reduction.Targeting viral antigens to CD11c on dendritic cells induces retrovirus-specific T cell responses A new role of the complement system: C3 provides protection in a mouse model of lung infection with intracellular Chlamydia psittaci.Complement mediated signaling on pulmonary CD103(+) dendritic cells is critical for their migratory function in response to influenza infection.Cooperativity between CD8+ T cells, non-neutralizing antibodies, and alveolar macrophages is important for heterosubtypic influenza virus immunity.Intranasal peptide-induced tolerance and linked suppression: consequences of complement deficiency The herpes simplex virus 1 IgG fc receptor blocks antibody-mediated complement activation and antibody-dependent cellular cytotoxicity in vivo.The Vaccinia virus complement control protein modulates adaptive immune responses during infection Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells.Impaired CD8(+) T cell immunity after allogeneic bone marrow transplantation leads to persistent and severe respiratory viral infection.Distinct contributions of vaccine-induced immunoglobulin G1 (IgG1) and IgG2a antibodies to protective immunity against influenza C3d adjuvant effects are mediated through the activation of C3d-specific autoreactive T cells Complement regulates CD4 T-cell help to CD8 T cells required for murine allograft rejection.

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P2860

Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection.

http://www.wikidata.org/entity/Q45733086

description

2002 nî lūn-bûn

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2002年の論文

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年學術文章

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2002年學術文章

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name

Complement component C3 promot ...... ute influenza virus infection.

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Complement component C3 promot ...... ute influenza virus infection.

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type

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Complement component C3 promot ...... ute influenza virus infection.

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Complement component C3 promot ...... ute influenza virus infection.

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Nature Medicine

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Complement component C3 promot ...... ute influenza virus infection.

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P2093

Brian Abel

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Martin F Bachmann

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Michael Carroll

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P2860

The C5a chemoattractant receptor mediates mucosal defence to infection

CD19: lowering the threshold for antigen receptor stimulation of B lymphocytes

C3d of complement as a molecular adjuvant: bridging innate and acquired immunity

Absence of marginal zone B cells in Pyk-2-deficient mice defines their role in the humoral response

Resistance to and recovery from lethal influenza virus infection in B lymphocyte-deficient mice.

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Anti-C5 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease.

Follicular dendritic cells as accessory cells.

Antibody response to a T-dependent antigen requires B cell expression of complement receptors

Protective T cell-independent antiviral antibody responses are dependent on complement.

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10.1038/NM0402-373

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