Evidence map›Paper›PMID 38563966›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

Recognition of Mycobacterium tuberculosis by macrophage Toll-like receptor and its role in autophagy.

Linna Wei, Liping Liu, Zudi Meng, Kai Qi, Xuehan Gao, Jihong Feng, Junmin Luo

Open access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Drug resistance mechanisms inFrontiers in pharmacology · 2026
    Review
  4. Review
  5. The Role of mTOR inBiomedicines · 2024
    Review
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

7 authors at 2 institutions in 1 country.

Linna WeiDepartment of Immunology, Zunyi Medical University, Zunyi, 563000, China.
Liping LiuDepartment of Immunology, Zunyi Medical University, Zunyi, 563000, China.
Zudi MengDepartment of Immunology, Zunyi Medical University, Zunyi, 563000, China.
Kai QiDepartment of Immunology, Zunyi Medical University, Zunyi, 563000, China.
Xuehan GaoDepartment of Immunology, Zunyi Medical University, Zunyi, 563000, China.
Jihong FengDepartment of Oncology, Lishui People's Hospital, Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, 323000, Zhejiang, China.
Junmin LuoDepartment of Immunology, Zunyi Medical University, Zunyi, 563000, China. luojm16128@163.com.
Zunyi Medical University · CNLishui City People's Hospital · CN

Funding

the funding support from the National Nature Science Foundation of China No. 81860291
6 · The paper itself

Abstract

backgroundThe pathogen responsible for tuberculosis is called Mycobacterium tuberculosis. Its interaction with macrophages has a significant impact on the onset and progression of the disease.

methodsThe respiratory pathway allows Mycobacterium tuberculosis to enter the body's lungs where it battles immune cells before being infected latently or actively. In the progress of tuberculosis, Mycobacterium tuberculosis activates the body's immune system and creates inflammatory factors, which cause tissue inflammation to infiltrate and the creation of granulomas, which seriously harms the body. Toll-like receptors of macrophage can mediate host recognition of Mycobacterium tuberculosis, initiate immune responses, and participate in macrophage autophagy. New host-directed therapeutic approaches targeting autophagy for drug-resistant Mycobacterium tuberculosis have emerged, providing new ideas for the effective treatment of tuberculosis.

conclusionsIn-depth understanding of the mechanisms by which macrophage autophagy interacts with intracellular Mycobacterium tuberculosis, as well as the study of potent and specific autophagy-regulating molecules, will lead to much-needed advances in drug discovery and vaccine design, which will improve the prevention and treatment of human tuberculosis.

Indexed as

AutophagyMacrophagesMycobacterium tuberculosisToll-Like ReceptorsTuberculosisAnimalsHumansToll-Like ReceptorsAutophagyMacrophageMycobacterium tuberculosisToll-like receptor

Identifiers

PMID38563966
OpenAlexW4393427108

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.