Evidence map›Paper›PMID 30524435›Full record

ArticleFrontiers in immunology2018

Regulating Innate and Adaptive Immunity for Controlling SIV Infection by 25-Hydroxycholesterol.

Tongjin Wu, Feng Ma, Xiuchang Ma, Weizhe Jia, Enxiang Pan, Genhong Cheng, Ling Chen, Caijun Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  7. A recombinantHuman vaccines & immunotherapeutics · 2023
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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 7 institutions in 2 countries.

Tongjin WuSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, China.
Feng MaCenter for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Xiuchang MaState Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Weizhe JiaSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, China.
Enxiang PanState Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Genhong ChengCenter for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Ling ChenState Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Caijun SunSchool of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, China.
Guangzhou Institutes of Biomedicine and Health · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Academy of Sciences · CNHebei University of Science and Technology · CNState Key Laboratory of Respiratory Disease · CNSun Yat-sen University · CNSuzhou Institute of Systems Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent inflammation and extensive immune activation have been associated with HIV-1/SIV pathogenesis. Previously, we reported that cholesterol-25-hydroxylase (CH25H) and its metabolite 25-hydroxycholesterol (25-HC) had a broad antiviral activity in inhibiting Zika, Ebola, and HIV-1 infection. However, the underlying immunological mechanism of CH25H and 25-HC in inhibiting viral infection remains poorly understood. We report here that 25-HC effectively regulates immune responses for controlling viral infection. CH25H expression was interferon-dependent and induced by SIV infection in monkey-derived macrophages and PBMC cells, and 25-HC inhibited SIV infection both in permissive cell lines and primary monkey lymphocytes. 25-HC also strongly inhibited bacterial lipopolysaccharide (LPS)-stimulated inflammation and restricted mitogen-stimulated proliferation in primary monkey lymphocytes. Strikingly, 25-HC promoted SIV-specific IFN-γ-producing cellular responses, but selectively suppressed proinflammatory CD4+ T lymphocytes secreting IL-2 and TNF-α cytokines in vaccinated mice. In addition, 25-HC had no significant immunosuppressive effects on cytotoxic CD8+ T lymphocytes or antibody-producing B lymphocytes. Collectively, 25-HC modulated both innate and adaptive immune responses toward inhibiting HIV/SIV infection. This study provides insights into improving vaccination and immunotherapy regimes against HIV-1 infection.

Indexed as

Immunity, CellularImmunity, InnateAnimalsCD4-Positive T-LymphocytesCell LineFemaleHydroxycholesterolsMacacaMacrophagesMiceMice, KnockoutSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusSteroid Hydroxylases25-hydroxycholesterolcholesterol 25-hydroxylaseHydroxycholesterolsSteroid Hydroxylases25-HCCTLHIV/SIVimmunotherapyinflammation

Identifiers

PMID30524435
PMCPMC6262225
OpenAlexW2901250898

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.