Evidence map›Paper›PMID 27511736›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Herpesvirus-Associated Lymphadenitis Distorts Fibroblastic Reticular Cell Microarchitecture and Attenuates CD8 T Cell Responses to Neurotropic Infection in Mice Lacking the STING-IFNα/β Defense Pathways.

Derek J Royer, Christopher D Conrady, Daniel J J Carr

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  8. Complement and CD4eLife · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Derek J RoyerDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; and Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104.ORCID 0000-0002-8476-1784
Christopher D ConradyDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; and.
Daniel J J CarrDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; and Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104 Dan-Carr@ouhsc.edu.
University of Oklahoma Health Sciences Center · US

Funding

P30-CENTER CORE GRANT FOR VISION RESEARCHP30EY021725 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Michelle C Callegan, MICHAEL H ELLIOTT · 2011 to 2026
$10.5M
The Neuroimmunology of Viral InfectionR01AI053108 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CARR, DANIEL J · 2003 to 2022
$5.8M
Vision Science Training ProgramT32EY023202 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CALLEGAN, MICHELLE C · 2014 to 2025
$952k
NEI NIH HHS P30 EY021725NEI NIH HHS T32 EY023202NIAID NIH HHS HHSN272201300006CNIAID NIH HHS R01 AI053108
6 · The paper itself

Abstract

Type I IFN (IFN-α/β)-driven immune responses to acute viral infection are critical to counter replication and prevent dissemination. However, the mechanisms underlying host resistance to HSV type 1 (HSV-1) are incompletely understood. In this study, we show that mice with deficiencies in IFN-α/β signaling or stimulator of IFN genes (STING) exhibit exacerbated neurovirulence and atypical lymphotropic dissemination of HSV-1 following ocular infection. Synergy between IFN-α/β signaling and efficacy of early adaptive immune responses to HSV-1 were dissected using bone marrow chimeras and adoptive cell transfer approaches to profile clonal expansion, effector function, and recruitment of HSV-specific CD8(+) T cells. Lymphotropic viral dissemination was commensurate with abrogated CD8(+) T cell responses and pathological alterations of fibroblastic reticular cell networks in the draining lymph nodes. Our results show that resistance to HSV-1 in the trigeminal ganglia during acute infection is conferred in part by STING and IFN-α/β signaling in both bone marrow-derived and -resident cells, which coalesce to support a robust HSV-1-specific CD8(+) T cell response.

Indexed as

Adaptive ImmunityAdoptive TransferAnimalsCD8-Positive T-LymphocytesEyeHerpes SimplexHerpesvirus 1, HumanInterferon-alphaInterferon beta-1aLymphadenitisMembrane ProteinsMiceSignal TransductionSTING ProteinTrigeminal GanglionVirus ReplicationInterferon-alphaInterferon beta-1aMembrane ProteinsSting1 protein, mouseSTING Protein

Identifiers

PMID27511736
PMCPMC5011016
OpenAlexW2515419740

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.