Evidence map›Paper›PMID 19825106›Full record

ReviewParasite immunology2009

Filariasis and lymphoedema.

K M Pfarr, A Y Debrah, S Specht, A Hoerauf

Open access · bronzeAbstract readReview
In one paragraph

Review in Parasite immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Biomaterials in the clinical treatment of lymphedema-a systematic review.Journal of vascular surgery. Venous and lymphatic disorders · 2024
    Pooled it
  2. Article
  3. Review
  4. Article
  5. From defense to disease: the multifaceted role of lymphatics during infection.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Podoconiosis in Uganda: prevalence, geographical distribution and risk factors.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2024
    Article
  11. Article
  12. Current Status of the Diagnosis ofPathogens (Basel, Switzerland) · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Domestic Dog as a Laboratory Host forPathogens (Basel, Switzerland) · 2022
    Article

8 more citing papers are in PubMed but not listed here.

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 1 institution in 2 countries.

K M PfarrInstitute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
A Y Debrah
S Specht
A Hoerauf
University Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among the causes of lymphoedema (LE), secondary LE due to filariasis is the most prevalent. It affects only a minority of the 120 million people infected with the causative organisms of lymphatic filariasis (LF), Wuchereria bancrofti and Brugia malayi/timori, but is clustered in families, indicating a genetic basis for development of this pathology. The majority of infected individuals develop filarial-specific immunosuppression that starts even before birth in cases where mothers are infected and is characterized by regulatory T-cell responses and high levels of IgG4, thus tolerating high parasite loads and microfilaraemia. In contrast, individuals with this pathology show stronger immune reactions biased towards Th1, Th2 and probably also Th17. Importantly, as for the aberrant lymph vessel development, innate immune responses that are triggered by the filarial antigen ultimately result in the activation of vascular endothelial growth factors (VEGF), thus promoting lymph vessel hyperplasia as a first step to lymphoedema development. Wolbachia endosymbionts are major inducers of these responses in vitro, and their depletion by doxycycline in LF patients reduces plasma VEGF and soluble VEGF-receptor-3 levels to those seen in endemic normals preceding pathology improvement. The search for the immunogenetic basis for LE could lead to the identification of risk factors and thus, to prevention; and has so far led to the identification of single-nucleotide polymorphisms (SNP) with potential functional relevance to VEGF, cytokine and toll-like receptor (TLR) genes. Hydrocele, a pathology with some similarity to LE in which both lymph vessel dilation and lymph extravasation are shared sequelae, has been found to be strongly associated with a VEGF-A SNP known for upregulation of this (lymph-)angiogenesis factor.

Indexed as

AnimalsElephantiasis, FilarialHumansImmune ToleranceImmunity, InnateLymphatic VesselsLymphedemaVascular Endothelial Growth Factor AWolbachiaVascular Endothelial Growth Factor A

Identifiers

PMID19825106
PMCPMC2784903
OpenAlexW1618459298

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.