Evidence map›Paper›PMID 31720742›Full record

ReviewCellular and molecular life sciences : CMLS2020

Host defense mechanisms against Mycobacterium tuberculosis.

Qiyao Chai, Zhe Lu, Cui Hua Liu

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

69 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  10. Peptide-Based Strategies AgainstPharmaceuticals (Basel, Switzerland) · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Progress of single-cell sequencing technology in immunotherapy for tuberculosis.Frontiers in cellular and infection microbiology · 2025
    Review
  18. Article
  19. The potential role and value of vitamin D in the treatment of tuberculosis.Frontiers in cellular and infection microbiology · 2025
    Review
  20. Article

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

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.

Qiyao ChaiCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China. chaiqy@im.ac.cn.
Zhe LuCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.
Cui Hua LiuCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China. liucuihua@im.ac.cn.ORCID http://orcid.org/0000-0002-8035-7792

Funding

Key Program of Logistics Research BWS17J030National Key Research and Development Program of China 2017YFA0505900National Natural Science Foundation of China 31830003National Natural Science Foundation of China 81571954National Natural Science Funds for Distinguished Young Scholar (81825014Strategic Priority Research Program of the Chinese Academy of Sciences XDB29020000
6 · The paper itself

Abstract

Tuberculosis (TB), which is caused by Mycobacterium tuberculosis (Mtb), remains the leading cause of death worldwide from a single infectious pathogen. Mtb is a paradigmatic intracellular pathogen that primarily invades the lungs after host inhalation of bacteria-containing droplets via the airway. However, the majority of Mtb-exposed individuals can spontaneously control the infection by virtue of a robust immune defense system. The mucosal barriers of the respiratory tract shape the first-line defense against Mtb through various mucosal immune responses. After arriving at the alveoli, the surviving mycobacteria further encounter a set of host innate immune cells that exert multiple cellular bactericidal functions. Adaptive immunity, predominantly mediated by a range of different T cell and B cell subsets, is subsequently activated and participates in host anti-mycobacterial defense. During Mtb infection, host bactericidal immune responses are exquisitely adjusted and balanced by multifaceted mechanisms, including genetic and epigenetic regulation, metabolic regulation and neuroendocrine regulation, which are indispensable for maintaining host immune efficiency and avoiding excessive tissue injury. A better understanding of the integrated and equilibrated host immune defense system against Mtb will contribute to the development of rational TB treatment regimens especially novel host-directed therapeutics.

Indexed as

Adaptive ImmunityB-LymphocytesEpigenesis, GeneticHIV InfectionsHost-Pathogen InteractionsHumansImmunity, InnateLungMycobacterium tuberculosisT-LymphocytesTuberculosisImmune checkpointsInnate-like T cellsInnate lymphoid cellsLung-resident immune cellsNeutrophilsTB-HIV co-infection

Identifiers

PMID31720742
PMCPMC11104961

What OpenQuestion holds

Textmetadata
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.