Evidence map›Paper›PMID 22110384›Full record

ArticleInternational journal of biological sciences2011

TLR2 mediates immunity to experimental cysticercosis.

José L Reyes, Marisol I González, Yadira Ledesma-Soto, Abhay R Satoskar, Luis I Terrazas

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in immunology · 2023
    Article
  4. Article
  5. Article
  6. Journal of immunology research · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Helminth-excreted/secreted products are recognized by multiple receptors on DCs to block the TLR response and bias Th2 polarization in a cRAF dependent pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  13. Immunoregulation by Taenia crassiceps and its antigens.BioMed research international · 2013
    Article
  14. Innate and cellular immunology in parasitic diseases.International journal of biological sciences · 2011
    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

5 authors at 2 institutions in 2 countries.

José L ReyesUnidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México-UNAM, Mexico.
Marisol I González
Yadira Ledesma-Soto
Abhay R Satoskar
Luis I Terrazas
Universidad Nacional Autónoma de México · MXThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Information concerning TLR-mediated antigen recognition and regulation of immune responses during helminth infections is scarce. TLR2 is a key molecule required for innate immunity and is involved in the recognition of a wide range of viruses, bacteria, fungi and parasites. Here, we evaluated the role of TLR2 in a Taenia crassiceps cysticercosis model. We compared the course of T. crassiceps infection in C57BL/6 TLR2 knockout mice (TLR2⁻/⁻) with that in wild type C57BL/6 (TLR2⁺/⁺) mice. In addition, we assessed serum antibody and cytokine profiles, splenic cellular responses and cytokine profiles and the recruitment of alternatively activated macrophages (AAMφs) to the site of the infection. Unlike wild type mice, TLR2⁻/⁻ mice failed to produce significant levels of inflammatory cytokines in either the serum or the spleen during the first two weeks of Taenia infection. TLR2⁻/⁻ mice developed a Th2-dominant immune response, whereas TLR2⁺/⁺ mice developed a Th1-dominant immune response after Taenia infection. The insufficient production of inflammatory cytokines at early time points and the lack of Th1-dominant adaptive immunity in TLR2⁻/⁻ mice were associated with significantly elevated parasite burdens; in contrast, TLR2⁺/⁺ mice were resistant to infection. Furthermore, increased recruitment of AAMφs expressing PD-L1, PD-L2, OX40L and mannose receptor was observed in TLR2⁻/⁻ mice. Collectively, these findings indicate that TLR2-dependent signaling pathways are involved in the recognition of T. crassiceps and in the subsequent activation of the innate immune system and production of inflammatory cytokines, which appear to be essential to limit infection during experimental cysticercosis.

Indexed as

AnimalsB7-H1 AntigenCell ProliferationCysticercosisEnzyme-Linked Immunosorbent AssayFlow CytometryLectins, C-TypeMannose-Binding LectinsMannose ReceptorMiceMice, Inbred C57BLMice, KnockoutOX40 LigandProgrammed Cell Death 1 Ligand 2 ProteinReceptors, Cell SurfaceTaeniaB7-H1 AntigenCd274 protein, mouseLectins, C-TypeMannose-Binding LectinsMannose ReceptorOX40 LigandPdcd1lg2 protein, mouseProgrammed Cell Death 1 Ligand 2 ProteinReceptors, Cell SurfaceTlr2 protein, mouseToll-Like Receptor 2alternatively activated macrophagescysticercosisTaenia crassicepsTLR2

Identifiers

PMID22110384
PMCPMC3221368
OpenAlexW2120493956

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.