Evidence map›Paper›PMID 27478636›Full record

ArticleChemotherapy research and practice2016

Interferon-Gamma Improves Macrophages Function against M. tuberculosis in Multidrug-Resistant Tuberculosis Patients.

Taj Ali Khan, Humaira Mazhar, Shamim Saleha, Hamid Nawaz Tipu, Niaz Muhammad, Muhammad Nasser Abbas

Open access · hybridAbstract read
In one paragraph

Article in Chemotherapy research and practice, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

44 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Journal of medical microbiology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. IFN-γ-Driven macrophage responses in the immunity toFrontiers in cellular and infection microbiology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Cytokine Responses duringMicroorganisms · 2023
    Article
  16. Article
  17. Pathogenicity of Type I Interferons inInternational journal of molecular sciences · 2023
    Review
  18. Article
  19. Article
  20. Early innate cell interactions withFrontiers in immunology · 2023
    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

6 authors at 2 institutions in 1 country.

Taj Ali KhanDepartment of Microbiology, Kohat University of Science and Technology, KPK, Kohat 26000, Pakistan.ORCID 0000-0002-0851-0422
Humaira MazharDepartment of Microbiology, Kohat University of Science and Technology, KPK, Kohat 26000, Pakistan.
Shamim SalehaDepartment of Biotechnology, Kohat University of Science and Technology, KPK, Kohat 26000, Pakistan.ORCID 0000-0002-1332-0666
Hamid Nawaz TipuDepartment of Immunology, Armed Forces Institute of Pathology, Rawalpindi 46000, Pakistan.ORCID 0000-0003-0105-103X
Niaz MuhammadDepartment of Microbiology, Kohat University of Science and Technology, KPK, Kohat 26000, Pakistan.
Muhammad Nasser AbbasDepartment of Microbiology, Kohat University of Science and Technology, KPK, Kohat 26000, Pakistan.
Kohat University of Science and Technology · PKArmed Forces Institute of Pathology · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background. Mycobacterium tuberculosis (M. tuberculosis) that causes tuberculosis (TB) kills millions of infected people annually especially multidrug-resistant tuberculosis (MDR-TB). On infection, macrophages recognize the mycobacteria by toll-like receptor (TLR) followed by phagocytosis and control of mycobacteria. In addition, macrophages also secrete IL-12 to induce IFN-γ production by T, which, in turn, increases the phagocytosis and oxidative burst. Individuals with defects in innate or adaptive immunity exhibit increased susceptibility to M. tuberculosis. Understanding these immunologic mechanisms will help in TB control. We aimed to investigate the immunopathologic mechanisms in MDR-TB and role of recombinant human interferon-gamma (rhIFN-γ). Study Design and Methods. Monocyte-derived macrophages (MDMs) were generated from peripheral blood mononuclear cells of MDR-TB patients and healthy subjects and were investigated for immunologic response by ELISA and flow cytometry. Results. Different functional and molecular anomalies were observed in macrophages. In addition, a defective immune response to M. tuberculosis from the patient's MDMs was characterized, which in turn improved by pretreatment with rhIFN-γ. Conclusion. This work highlights the fact that rhIFN-γ improves macrophages function against M. tuberculosis and treatment of patients with poor responsiveness to TB therapy may be needed in future to include IFN-γ as adjuvant therapy after the full characterization of pathological and molecular mechanisms in these and in other more multidrug-resistant TB patients.

Identifiers

PMID27478636
PMCPMC4960331
OpenAlexW2466236852

What OpenQuestion holds

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LicenceCC BY
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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.