Evidence map›Paper›PMID 25500584›Full record

ArticlePLoS pathogens2014

Expression of suppressor of cytokine signaling 1 (SOCS1) impairs viral clearance and exacerbates lung injury during influenza infection.

Keer Sun, Sharon Salmon, Vijaya Kumar Yajjala, Christopher Bauer, Dennis W Metzger

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 27% 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, 27 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Keer SunCenter for Immunology and Microbial Disease, Albany Medical College, Albany, New York, United States of America; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Sharon SalmonCenter for Immunology and Microbial Disease, Albany Medical College, Albany, New York, United States of America.
Vijaya Kumar YajjalaDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Christopher BauerDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Dennis W MetzgerCenter for Immunology and Microbial Disease, Albany Medical College, Albany, New York, United States of America.
University of Nebraska Medical Center · USAlbany Medical Center Hospital · US

Funding

Oxidative Burst in Influenza and MRSA Co-infectionR01HL118408 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SUN, KEER · 2013 to 2022
$3.9M
Identification of genes that affect peak BMD in men and womenR01AG041517 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI ECONS, MICHAEL J · 2011 to 2015
$2.9M
Effect of Influenza Infection on Alveolar Macrophage FunctionR01AI075312 · NIAID · ALBANY MEDICAL COLLEGE · PI METZGER, DENNIS W · 2009 to 2012
$1.6M
NHLBI NIH HHS R01 HL118408NIAID NIH HHS HHSN272201300006CNIAID NIH HHS R01 AI075312NIAID NIH HHS R01 AI41517NIAID NIH HHS R01 AI75312NIA NIH HHS R01 AG041517
6 · The paper itself

Abstract

Suppressor of cytokine signaling (SOCS) proteins are inducible feedback inhibitors of cytokine signaling. SOCS1-/- mice die within three weeks postnatally due to IFN-γ-induced hyperinflammation. Since it is well established that IFN-γ is dispensable for protection against influenza infection, we generated SOCS1-/-IFN-γ-/- mice to determine whether SOCS1 regulates antiviral immunity in vivo. Here we show that SOCS1-/-IFN-γ-/- mice exhibited significantly enhanced resistance to influenza infection, as evidenced by improved viral clearance, attenuated acute lung damage, and consequently increased survival rates compared to either IFN-γ-/- or WT animals. Enhanced viral clearance in SOCS1-/-IFN-γ-/- mice coincided with a rapid onset of adaptive immune responses during acute infection, while their reduced lung injury was associated with decreased inflammatory cell infiltration at the resolution phase of infection. We further determined the contribution of SOCS1-deficient T cells to antiviral immunity. Anti-CD4 antibody treatment of SOCS1-/-IFN-γ-/- mice had no significant effect on their enhanced resistance to influenza infection, while CD8+ splenocytes from SOCS1-/-IFN-γ-/- mice were sufficient to rescue RAG1-/- animals from an otherwise lethal infection. Surprisingly, despite their markedly reduced viral burdens, RAG1-/- mice reconstituted with SOCS1-/-IFN-γ-/- adaptive immune cells failed to ameliorate influenza-induced lung injury. In conclusion, in the absence of IFN-γ, the cytoplasmic protein SOCS1 not only inhibits adaptive antiviral immune responses but also exacerbates inflammatory lung damage. Importantly, these detrimental effects of SOCS1 are conveyed through discrete cell populations. Specifically, while SOCS1 expression in adaptive immune cells is sufficient to inhibit antiviral immunity, SOCS1 in innate/stromal cells is responsible for aggravated lung injury.

Indexed as

Adaptive ImmunityAnimalsCytokinesDisease Models, AnimalHomeodomain ProteinsInterferon-gammaLung DiseasesLung InjuryMiceMice, Inbred C57BLMice, KnockoutOrthomyxoviridaeOrthomyxoviridae InfectionsSignal TransductionSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsCytokinesHomeodomain ProteinsInterferon-gammaRAG-1 proteinSocs1 protein, mouseSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID25500584
PMCPMC4263766
OpenAlexW2084995639

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.