Evidence map›Paper›PMID 26041993›Full record

ReviewFrontiers in cellular neuroscience2015

Microglia are crucial regulators of neuro-immunity during central nervous system tuberculosis.

Jonathan Paul Spanos, Nai-Jen Hsu, Muazzam Jacobs

Abstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  9. Review
  10. Ocular mycobacterial lesions in cats.Veterinary pathology · 2022
    Article
  11. Affinity of Mycobacterium tuberculosis strains for M059K microglial cells after migration through A549 alveolar epithelium.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Frontiers in cellular and infection microbiology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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.

Jonathan Paul SpanosDivision of Immunology, Faculty of Health Sciences, Institute of Infectious Disease and Molecular Medicine, University of Cape Town Cape Town, South Africa.
Nai-Jen HsuDivision of Immunology, Faculty of Health Sciences, Institute of Infectious Disease and Molecular Medicine, University of Cape Town Cape Town, South Africa.
Muazzam JacobsDivision of Immunology, Faculty of Health Sciences, Institute of Infectious Disease and Molecular Medicine, University of Cape Town Cape Town, South Africa ; National Health Laboratory Service Johannesburg, South Africa.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis (M. tuberculosis) infection of the central nervous system (CNS) is the most devastating manifestation of tuberculosis (TB), with both high mortality and morbidity. Although research has been fueled by the potential therapeutic target microglia offer against neurodegenerative inflammation, their part in TB infection of the CNS has not been fully evaluated nor elucidated. Yet, as both the preferential targets of M. tuberculosis and the immune-effector cells of the CNS, microglia are likely to be key determinants of disease severity and clinical outcomes. Following pathogen recognition, bacilli are internalized and capable of replicating within microglia. Cellular activation ensues, utilizing signaling molecules that may be neurotoxic. Central to initiating, orchestrating and modulating the tuberculous immune response is microglial secretion of cytokines and chemokines. However, the neurological environment is unique in that inflammatory signals, which appear to be damaging in the periphery, could be beneficial by governing neuronal survival, regeneration and differentiation. Furthermore, microglia are important in the recruitment of peripheral immune cells and central to defining the pro-inflammatory milieu of which neurotoxicity may result from many of the participating local or recruited cell types. Microglia are capable of both presenting antigen to infiltrating CD4(+) T-lymphocytes and inducing their differentiation-a possible correlate of protection against M. tuberculosis infection. Clarifying the nature of the immune effector molecules secreted by microglia, and the means by which other CNS-specific cell types govern microglial activation or modulate their responses is critical if improved diagnostic and therapeutic strategies are to be attained. Therefore, this review evaluates the diverse roles microglia play in the neuro-immunity to M. tuberculosis infection of the CNS.

Indexed as

central nervous systemchemokinescytokinesmicrogliaMycobacterium tuberculosisneuroprotectionneurotoxicitytuberculosis meningitis

Identifiers

PMID26041993
PMCPMC4435040

What OpenQuestion holds

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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.