Evidence map›Paper›PMID 33720048›Full record

ArticleThe Journal of clinical investigation2021

NLRP3 inflammasome induces CD4+ T cell loss in chronically HIV-1-infected patients.

Chao Zhang, Jin-Wen Song, Hui-Huang Huang, Xing Fan, Lei Huang, Jian-Ning Deng, Bo Tu, Kun Wang, Jing Li, Ming-Ju Zhou and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
8.8field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 136 citations in OpenAlex.

  1. Review
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  14. Review
  15. Targeting inflammasomes as a therapeutic potential for HIV/AIDS.Cellular and molecular life sciences : CMLS · 2025
    Review
  16. Article
  17. Review
  18. Article
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  20. Review

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 2 countries.

Chao ZhangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Jin-Wen SongDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Hui-Huang HuangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Xing FanDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Lei HuangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Jian-Ning DengGuangxi AIDS Clinical Treatment Center, The Fourth People's Hospital of Nanning, Nanning, Guangxi, China.
Bo TuDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Kun WangNational Institute of Biological Sciences, Beijing, China.
Jing LiDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Ming-Ju ZhouDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Cui-Xian YangYunnan Infectious Disease Hospital, Kunming, China.
Qi-Wen ZhaoDepartment of Pathology, Sixth Medical Center of Chinese PLA General Hospital, Beijing, China.
Tao YangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Li-Feng WangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Ji-Yuan ZhangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Ruo-Nan XuDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Yan-Mei JiaoDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Ming ShiDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Feng ShaoNational Institute of Biological Sciences, Beijing, China.
Rafick-Pierre SékalyDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.
Fu-Sheng WangDepartment of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital, National Clinical Research Center for Infectious Diseases, Beijing, China.
Chinese PLA General Hospital · CNNational Institute of Biological Sciences, Beijing · CNCase Western Reserve University · USKunming Third People's Hospital · CNThe Second Nanning People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic HIV-1 infection is generally characterized by progressive CD4+ T cell depletion due to direct and bystander death that is closely associated with persistent HIV-1 replication and an inflammatory environment in vivo. The mechanisms underlying the loss of CD4+ T cells in patients with chronic HIV-1 infection are incompletely understood. In this study, we simultaneously monitored caspase-1 and caspase-3 activation in circulating CD4+ T cells, which revealed that pyroptotic and apoptotic CD4+ T cells are distinct cell populations with different phenotypic characteristics. Levels of pyroptosis and apoptosis in CD4+ T cells were significantly elevated during chronic HIV-1 infection, and decreased following effective antiretroviral therapy. Notably, the occurrence of pyroptosis was further confirmed by elevated gasdermin D activation in lymph nodes of HIV-1-infected individuals. Mechanistically, caspase-1 activation closely correlated with the inflammatory marker expression and was shown to occur through NLRP3 inflammasome activation driven by virus-dependent and/or -independent ROS production, while caspase-3 activation in CD4+ T cells was more closely related to T cell activation status. Hence, our findings show that NLRP3-dependent pyroptosis plays an essential role in CD4+ T cell loss in HIV-1-infected patients and implicate pyroptosis signaling as a target for anti-HIV-1 treatment.

Indexed as

HIV-1AdolescentAdultApoptosisCase-Control StudiesCaspase 1Caspase 3CD4-Positive T-LymphocytesFemaleHIV InfectionsHumansInflammasomesLymphocyte ActivationMaleMiddle AgedModels, ImmunologicalCASP3 protein, humanCaspase 1Caspase 3InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanReactive Oxygen SpeciesAIDS/HIVCaspases and caspase substratesInflammationT cells

Identifiers

PMID33720048
PMCPMC7954596
OpenAlexW3139209701

What OpenQuestion holds

Textmetadata
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Registered trials

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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.