Evidence map›Paper›PMID 24600029›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Intrahepatic innate lymphoid cells secrete IL-17A and IL-17F that are crucial for T cell priming in viral infection.

Zuliang Jie, Yuejin Liang, Lifei Hou, Chen Dong, Yoichiro Iwakura, Lynn Soong, Yingzi Cong, Jiaren Sun

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

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  14. Clonal Vγ6Proceedings of the National Academy of Sciences of the United States of America · 2019
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  17. NCREBioMedicine · 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

8 authors at 3 institutions in 2 countries.

Zuliang JieDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555;
Yuejin Liang
Lifei Hou
Chen Dong
Yoichiro Iwakura
Lynn Soong
Yingzi Cong
Jiaren Sun
The University of Texas Medical Branch at Galveston · USNoda Institute for Scientific Research · JPThe University of Texas MD Anderson Cancer Center · US

Funding

Immune Mechanisms of HCV Persistence and PathogenesisR01AI069142 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SUN, JIAREN · 2007 to 2012
$2.0M
NIAID NIH HHS AI69142NIAID NIH HHS R01 AI069142
6 · The paper itself

Abstract

Intrahepatic cell-derived, early IL-17 is important for activating APCs in viral infection; however, the source and regulation of this IL-17 surge in the liver microenvironment are not well defined. In this article, we present evidence for a significant expansion of IL-17A/F-producing cells in mouse liver within 24 h of adenovirus infection. In addition to γδ T cells, a subset of IL-17A/F(+) cells expressed no myeloid or lymphoid lineage markers. Instead, they expressed high levels of stem cell markers, IL-7R and RORγt, consistent with the newly described innate lymphoid cells (ILCs). Based on their unique surface markers and cytokine profiles, these cells were confirmed as group 3 ILCs. In addition to adenovirus infection, group 3 ILCs were also found in mouse liver within 24 h of lymphocytic choriomeningitis virus infection. They contributed significantly to the establishment of the early cytokine milieu in virus-infected liver. Functional studies with mice deficient of IL-17R, IL-17A, and IL-17F further revealed that IL-17 signaling was critical for priming T cell responses in viral hepatitis. IL-17A repressed IL-17F secretion in vitro and in vivo; IL-17F(+) intrahepatic cells expanded more vigorously in IL-17A knockout animals, permitting efficient Ag presentation and T cell function. However, IL-17F neither inhibited IL-17A in vitro nor regulated its secretion in vivo. Together, this study has demonstrated the importance of a unique intrahepatic subpopulation and subsequent IL-17A/F regulation at initial stages of viral infection in the liver. These results have important implications for anticytokine biologic therapy and vaccine development.

Indexed as

AdenoviridaeAnimalsCells, CulturedChemokine CXCL10Chemokine CXCL9FemaleFlow CytometryHost-Pathogen InteractionsInterferon-gammaInterleukin-17LiverLymphocytesLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, KnockoutChemokine CXCL10Chemokine CXCL9Il17ra protein, mouseInterferon-gammaInterleukin-17Receptors, Antigen, T-Cell, gamma-deltaReceptors, Interleukin-17Tumor Necrosis Factor-alpha

Identifiers

PMID24600029
PMCPMC3967589
OpenAlexW2128674254

What OpenQuestion holds

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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.