Evidence map›Paper›PMID 26272216›Full record

ArticleBlood2015

DC-SIGN-expressing macrophages trigger activation of mannosylated IgM B-cell receptor in follicular lymphoma.

Rada Amin, Frédéric Mourcin, Fabrice Uhel, Céline Pangault, Philippe Ruminy, Loic Dupré, Marion Guirriec, Tony Marchand, Thierry Fest, Thierry Lamy and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

78 citing papers in PubMed, 130 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Rada AminEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France;
Frédéric MourcinEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France;
Fabrice UhelEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Service de réanimation médicale, Centre Hospitalier Universitaire de Rennes, Rennes, France;
Céline PangaultEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France; Pôle Biologie, Centre Hospitalier Universitaire de Rennes, Rennes, France;
Philippe RuminyCentre Henri Becquerel, Université de Rouen, Unité Mixte de Recherche U918, INSERM, Rouen, France;
Loic DupréUniversité Toulouse III Paul-Sabatier, Toulouse, France; Centre de Physiopathologie de Toulouse Purpan, Unité Mixte de Recherche 1043, INSERM, Toulouse, France; and.
Marion GuirriecEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France;
Tony MarchandEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France; Service d'Hématologie Clinique, Centre Hospitalier Universitaire de Rennes, Rennes, France.
Thierry FestEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France; Pôle Biologie, Centre Hospitalier Universitaire de Rennes, Rennes, France;
Thierry LamyEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France; Service d'Hématologie Clinique, Centre Hospitalier Universitaire de Rennes, Rennes, France.
Karin TarteEquipe Labellisée Ligue Contre le Cancer, Unité Mixte de Recherche U917, INSERM, Rennes, France; Université Rennes 1, Unité Mixte de Recherche U917, Rennes, France; Etablissement Français du Sang Bretagne, Rennes, France; Pôle Biologie, Centre Hospitalier Universitaire de Rennes, Rennes, France;ORCID http://orcid.org/0000-0002-6809-917X
Inserm · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Follicular lymphoma (FL) results from the accumulation of malignant germinal center (GC) B cells leading to the development of an indolent and largely incurable disease. FL cells remain highly dependent on B-cell receptor (BCR) signaling and on a specific cell microenvironment, including T cells, macrophages, and stromal cells. Importantly, FL BCR is characterized by a selective pressure to retain surface immunoglobulin M (IgM) BCR despite an active class-switch recombination process, and by the introduction, in BCR variable regions, of N-glycosylation acceptor sites harboring unusual high-mannose oligosaccharides. However, the relevance of these 2 FL BCR features for lymphomagenesis remains unclear. In this study, we demonstrated that IgM(+) FL B cells activated a stronger BCR signaling network than IgG(+) FL B cells and normal GC B cells. BCR expression level and phosphatase activity could both contribute to such heterogeneity. Moreover, we underlined that a subset of IgM(+) FL samples, displaying highly mannosylated BCR, efficiently bound dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN), which could in turn trigger delayed but long-lasting BCR aggregation and activation. Interestingly, DC-SIGN was found within the FL cell niche in situ. Finally, M2 macrophages induced a DC-SIGN-dependent adhesion of highly mannosylated IgM(+) FL B cells and triggered BCR-associated kinase activation. Interestingly, pharmacologic BCR inhibitors abolished such crosstalk between macrophages and FL B cells. Altogether, our data support an important role for DC-SIGN-expressing infiltrating cells in the biology of FL and suggest that they could represent interesting therapeutic targets.

Indexed as

Cell Adhesion MoleculesCell CommunicationCoculture TechniquesDC-Specific ICAM-3 Grabbing NonintegrinFemaleGene Expression RegulationGlycosylationHumansImmunoglobulin MLectins, C-TypeLymphoma, FollicularMacrophagesMaleReceptors, Antigen, B-CellReceptors, Cell SurfaceSignal TransductionCell Adhesion MoleculesDC-Specific ICAM-3 Grabbing NonintegrinImmunoglobulin MLectins, C-TypeReceptors, Antigen, B-CellReceptors, Cell Surface

Identifiers

PMID26272216
PMCPMC4626662
OpenAlexW1779052524

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.