Evidence map›Paper›PMID 22511870›Full record

ArticlePLoS pathogens2012

TLR4 and NKT cell synergy in immunotherapy against visceral leishmaniasis.

Subir Karmakar, Siddhartha Kumar Bhaumik, Joydeep Paul, Tripti De

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 57 citations in OpenAlex.

  1. Frontiers in immunology · 2023
    Review
  2. Unwinding the mechanism of macrophage repolarization potential ofFrontiers in cellular and infection microbiology · 2023
    Article
  3. Review
  4. Article
  5. The iNKT Cell-Macrophage Axis in Homeostasis and Disease.International journal of molecular sciences · 2022
    Review
  6. Role of Cytokines in Experimental and Human Visceral Leishmaniasis.Frontiers in cellular and infection microbiology · 2021
    Review
  7. Review
  8. License to Kill: When iNKT Cells Are Granted the Use of Lethal Cytotoxicity.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Neutrophil elastase promotesFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Review
  12. Article
  13. Frontiers in immunology · 2017
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

4 authors at 2 institutions in 1 country.

Subir KarmakarDivision of Infectious Disease and Immunology, Indian Institute of Chemical Biology, Council of Scientific and Industrial Research, Kolkata, India.
Siddhartha Kumar Bhaumik
Joydeep Paul
Tripti De
Council of Scientific and Industrial Research · INIndian Institute of Chemical Biology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NKT cells play an important role in autoimmune diseases, tumor surveillance, and infectious diseases, providing in most cases protection against infection. NKT cells are reactive to CD1d presented glycolipid antigens. They can modulate immune responses by promoting the secretion of type 1, type 2, or immune regulatory cytokines. Pathogen-derived signals to dendritic cells mediated via Toll like Receptors (TLR) can be modulated by activated invariant Natural Killer T (iNKT) cells. The terminal β-(1-4)-galactose residues of glycans can modulate host responsiveness in a T helper type-1 direction via IFN-γ and TLRs. We have attempted to develop a defined immunotherapeutic, based on the cooperative action of a TLR ligand and iNKT cell using a mouse model of visceral leishmaniasis. We evaluated the anti-Leishmania immune responses and the protective efficacy of the β-(1-4)-galactose terminal NKT cell ligand glycosphingophospholipid (GSPL) antigen of L. donovani parasites. Our results suggest that TLR4 can function as an upstream sensor for GSPL and provoke intracellular inflammatory signaling necessary for parasite killing. Treatment with GSPL was able to induce a strong effective T cell response that contributed to effective control of acute parasite burden and led to undetectable parasite persistence in the infected animals. These studies for the first time demonstrate the interactions between a TLR ligand and iNKT cell activation in visceral leishmaniasis immunotherapeutic.

Indexed as

AnimalsAntigen PresentationAntigens, CD1dAntigens, ProtozoanCricetinaeGlycosphingolipidsImmunotherapyLeishmania donovaniLeishmaniasis, VisceralMiceMice, Inbred BALB CNatural Killer T-CellsPolysaccharidesTh1 CellsToll-Like Receptor 4Antigens, CD1dAntigens, ProtozoanCd1d1 protein, mouseGlycosphingolipidsPolysaccharidesTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID22511870
PMCPMC3325212
OpenAlexW2059125127

What OpenQuestion holds

Textmetadata
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.