Type I interferon is selectively required by dendritic cells for immune rejection of tumors (Q28248500)

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Hirokazu Matsushita

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Mona Mashayekhi

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Gavin P Dunn

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Jessica M Archambault

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Hsiaoju Lee

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Cora D Arthur

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Kenneth M Murphy

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Robert D Schreiber

Journal of Experimental Medicine

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language of work or name

English

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publication date

26 September 2011

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published in

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volume

208

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issue

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page(s)

1989-2003

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cites work

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Type I IFN receptor signals directly stimulate local B cells early following influenza virus infection

21 January 2018

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A critical function for type I interferons in cancer immunoediting

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Prognostic significance of autoimmunity during treatment of melanoma with interferon.

21 January 2018

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Adaptive immunity maintains occult cancer in an equilibrium state

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Establishment of monoclonal anti-Nk-1.1 antibody.

21 January 2018

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Cross-priming of CD8+ T cells stimulated by virus-induced type I interferon

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Cutting edge: enhancement of antibody responses through direct stimulation of B and T cells by type I IFN.

21 January 2018

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Type I IFNs control antigen retention and survival of CD8α(+) dendritic cells after uptake of tumor apoptotic cells leading to cross-priming

21 January 2018

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Dendritic cells require STAT-1 phosphorylated at its transactivating domain for the induction of peptide-specific CTL.

21 January 2018

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Distinct and Nonredundant In Vivo Functions of IFNAR on Myeloid Cells Limit Autoimmunity in the Central Nervous System

21 January 2018

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CD4+ T cell--mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFN gamma receptor expression by nonhematopoietic cells.

21 January 2018

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https://api.crossref.org/works/10.1084%2FJEM.20101158

Blocking Monoclonal Antibodies Specific for Mouse IFN-α/β Receptor Subunit 1 (IFNAR-1) from Mice Immunized by In Vivo Hydrodynamic Transfection

21 January 2018

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https://api.crossref.org/works/10.1084%2FJEM.20101158

Bystander elimination of antigen loss variants in established tumors

21 January 2018

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https://api.crossref.org/works/10.1084%2FJEM.20101158

Innate inflammatory signals induced by various pathogens differentially dictate the IFN-I dependence of CD8 T cells for clonal expansion and memory formation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1084%2FJEM.20101158

Type I IFNs enhance the terminal differentiation of dendritic cells

21 January 2018

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Therapy with monoclonal antibodies by elimination of T-cell subsets in vivo

27 November 2018

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Roles of tumour localization, second signals and cross priming in cytotoxic T-cell induction

21 January 2018

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Redundancy of direct priming and cross-priming in tumor-specific CD8+ T cell responses

21 January 2018

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12 December 2020

Type I interferons produced by dendritic cells promote their phenotypic and functional activation

1 reference

12 December 2020

Coordinated and distinct roles for IFN-alpha beta, IL-12, and IL-15 regulation of NK cell responses to viral infection

1 reference

12 December 2020

Characterization of the murine T cell surface molecule, designated L3T4, identified by monoclonal antibody GK1.5: similarity of L3T4 to the human Leu-3/T4 molecule

1 reference

12 December 2020

Type I IFNs provide a third signal to CD8 T cells to stimulate clonal expansion and differentiation

1 reference

12 December 2020

Direct Stimulation of T Cells by Type I IFN Enhances the CD8+ T Cell Response during Cross-Priming

1 reference

12 December 2020

Type I interferons directly regulate lymphocyte recirculation and cause transient blood lymphopenia

1 reference

12 December 2020

Type I IFN contributes to NK cell homeostasis, activation, and antitumor function

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12 December 2020

Identifiers

DOI

10.1084/JEM.20101158

1 reference

1 reference

1 reference

PubMed publication ID

21930769

1 reference