Evidence map›Paper›PMID 28899929›Full record

ArticleEMBO molecular medicine2017

Pathogen-specific B-cell receptors drive chronic lymphocytic leukemia by light-chain-dependent cross-reaction with autoantigens.

Nereida Jiménez de Oya, Marco De Giovanni, Jessica Fioravanti, Rudolf Übelhart, Pietro Di Lucia, Amleto Fiocchi, Stefano Iacovelli, Dimitar G Efremov, Federico Caligaris-Cappio, Hassan Jumaa and 3 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-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

16 citing papers in PubMed, 19 citations in OpenAlex.

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  7. TheFrontiers in immunology · 2021
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  13. PD-L1 over-expression is driven by B-cell receptor signaling in diffuse large B-cell lymphoma.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
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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

13 authors at 4 institutions in 2 countries.

Nereida Jiménez de OyaDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Marco De GiovanniDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Jessica FioravantiDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Rudolf ÜbelhartInstitute of Immunology, University Hospital Ulm, Ulm, Germany.
Pietro Di LuciaDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Amleto FiocchiDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Stefano IacovelliMolecular Hematology Unit, International Centre for Genetic Engineering & Biotechnology, Trieste, Italy.
Dimitar G EfremovMolecular Hematology Unit, International Centre for Genetic Engineering & Biotechnology, Trieste, Italy.
Federico Caligaris-CappioDivision of Experimental Oncology, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Hassan JumaaInstitute of Immunology, University Hospital Ulm, Ulm, Germany.ORCID 0000-0003-3383-141X
Paolo GhiaVita-Salute San Raffaele University, Milan, Italy.
Luca G GuidottiDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Matteo IannaconeDivision of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy iannacone.matteo@hsr.it.ORCID 0000-0002-9370-2671
Vita-Salute San Raffaele University · ITInternational Centre for Genetic Engineering and Biotechnology · ITUniversity Hospital Ulm · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several lines of evidence indirectly suggest that antigenic stimulation through the B-cell receptor (BCR) supports chronic lymphocytic leukemia (CLL) development. In addition to self-antigens, a number of microbial antigens have been proposed to contribute to the selection of the immunoglobulins expressed in CLL. How pathogen-specific BCRs drive CLL development remains, however, largely unexplored. Here, we utilized mouse models of CLL pathogenesis to equip B cells with virus-specific BCRs and study the effect of antigen recognition on leukemia growth. Our results show that BCR engagement is absolutely required for CLL development. Unexpectedly, however, neither acute nor chronic exposure to virus-derived antigens influenced leukemia progression. Rather, CLL clones preferentially selected light chains that, when paired with virus-specific heavy chains, conferred B cells the ability to recognize a broad range of autoantigens. Taken together, our results suggest that pathogens may drive CLL pathogenesis by selecting and expanding pathogen-specific B cells that cross-react with one or more self-antigens.

Indexed as

Amino Acid SequenceAnimalsAutoantigensDisease Models, AnimalImmunoglobulin Light ChainsImmunoglobulinsIntercellular Adhesion Molecule-3Leukemia, Lymphocytic, Chronic, B-CellMaleMiceMice, Inbred C57BLMice, TransgenicProtein Array AnalysisProto-Oncogene ProteinsReceptors, Antigen, B-CellSpleenAutoantigensImmunoglobulin Light ChainsImmunoglobulinsIntercellular Adhesion Molecule-3Proto-Oncogene ProteinsReceptors, Antigen, B-CellTCL1A protein, humanautoantigensB‐cell receptorchronic lymphocytic leukemiainfectionlight chains

Identifiers

PMID28899929
PMCPMC5666309
OpenAlexW2756143144

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.