Evidence map›Paper›PMID 20407205›Full record

ArticleThe Journal of clinical investigation2010

Mannose receptor interacts with Fc receptors and is critical for the development of crescentic glomerulonephritis in mice.

Konstantia-Maria Chavele, Luisa Martinez-Pomares, Jan Domin, Samantha Pemberton, Stuart M Haslam, Anne Dell, H Terence Cook, Charles D Pusey, Siamon Gordon, Alan D Salama

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. 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
3.4field-weighted citation impact, top 7% 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, 65 citations in OpenAlex.

  1. Article
  2. NLRP3 inflammasome activity and pyroptosis are involved in CD206Acta biochimica et biophysica Sinica · 2025
    Article
  3. Article
  4. Article
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  7. Review
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  12. Article
  13. Autoantibody-induced internalization of CNS AQP4 water channel and EAAT2 glutamate transporter requires astrocytic Fc receptor.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014
    Review
  19. Article
  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

10 authors at 4 institutions in 2 countries.

Konstantia-Maria ChaveleRenal Section, Division of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Luisa Martinez-Pomares
Jan Domin
Samantha Pemberton
Stuart M Haslam
Anne Dell
H Terence Cook
Charles D Pusey
Siamon Gordon
Alan D Salama
Imperial College London · GBHammersmith Hospital · GBQueen's Medical Centre · GBUniversity of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council B19088Biotechnology and Biological Sciences Research Council BBF0083091Medical Research Council G0500936
6 · The paper itself

Abstract

Crescentic glomerulonephritis (CGN), which frequently results in acute and chronic kidney disease, is characterized by and dependent on glomerular infiltration by macrophages. The mannose receptor (MR) is a pattern recognition receptor implicated in the uptake of endogenous and microbial ligands by macrophages, mesangial cells (MCs), and selected endothelial cells. It is upregulated on alternatively activated macrophages (i.e., macrophages associated with tissue repair and humoral immunity) and involved in antigen presentation to T cells. We used the mouse model of nephrotoxic nephritis to investigate the role of MR in CGN. Our results demonstrate what we believe to be a novel role for MR in the promotion of CGN that is independent of adaptive immune responses. MR-deficient (Mr-/-) mice were protected from CGN despite generating humoral and T cell responses similar to those of WT mice, but they demonstrated diminished macrophage and MC Fc receptor-mediated (FcR-mediated) functions, including phagocytosis and Fc-mediated oxygen burst activity. Mr-/- MCs demonstrated augmented apoptosis compared with WT cells, and this was associated with diminished Akt phosphorylation. Macrophage interaction with apoptotic MCs induced a noninflammatory phenotype that was more marked in Mr-/- macrophages than in WT macrophages. Our results demonstrate that MR augments Fc-mediated function and promotes MC survival. We suggest that targeting MR may provide an alternative therapeutic approach in CGN while minimizing the impact on adaptive immune responses, which are affected by conventional immunosuppressive approaches.

Indexed as

Gene Expression RegulationAnimalsApoptosisFemaleGlomerulonephritisLectins, C-TypeMacrophagesMaleMannose-Binding LectinsMannose ReceptorMesangial CellsMiceMice, Inbred C57BLMice, TransgenicModels, BiologicalOxygenLectins, C-TypeMannose-Binding LectinsMannose ReceptorOxygenReceptors, Cell SurfaceReceptors, Fc

Identifiers

PMID20407205
PMCPMC2860943
OpenAlexW2084264383

What OpenQuestion holds

Textmetadata
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.