Evidence map›Paper›PMID 29416129›Full record

ReviewNature reviews. Rheumatology2018

B cells in the pathogenesis of primary Sjögren syndrome.

Gaëtane Nocturne, Xavier Mariette

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed, 4 pooled it
15.3field-weighted citation impact, top 1% 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

210 citing papers in PubMed, 4 syntheses or guidelines pooled it, 342 citations in OpenAlex.

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  20. Molecular Insights into Oral Manifestations in Sjögren's Disease.International journal of molecular sciences · 2026
    Review

150 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

2 authors at 2 institutions in 1 country.

Gaëtane NocturneDepartment of Rheumatology, Université Paris-Sud, INSERM U1184: Centre for Immunology of Viral Infections and Autoimmune Diseases, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpitaux Universitaires Paris-Sud Bicêtre, Le Kremlin-Bicêtre, France.
Xavier MarietteDepartment of Rheumatology, Université Paris-Sud, INSERM U1184: Centre for Immunology of Viral Infections and Autoimmune Diseases, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpitaux Universitaires Paris-Sud Bicêtre, Le Kremlin-Bicêtre, France.
Assistance Publique – Hôpitaux de Paris · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary Sjögren syndrome (pSS) is a prototypical autoimmune disease. The involvement of B cells in the pathogenesis of pSS has long been suspected on the basis of clinical observations that include the presence of serum autoantibodies, hypergammaglobulinaemia, increased levels of free light chains and increased risk of B cell lymphoma. Moreover, the composition of the B cell subset is altered in pSS. In this Review, we discuss the mechanisms that support the increased activation of B cells in pSS, including genetic and epigenetic factors and environmental triggers that promote B cell activation via the innate immune system. B cell activating factor (BAFF, also known as TNF ligand superfamily member 13B) is at the crossroads of this process. An important role also exists for the target tissue (exocrine glands, namely the salivary and lachrymal glands), which promotes local B cell activation. This continuous stimulation of B cells is the main driver of lymphomatous escape. Identification of the multiple steps that support B cell activation has led to the development of promising targeted therapies that will hopefully lead to the development of an efficient therapeutic strategy for pSS.

Indexed as

B-Cell Activating FactorB-LymphocytesEpigenesis, GeneticGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLymphocyte ActivationSjogren's SyndromeB-Cell Activating FactorTNFSF13B protein, human

Identifiers

PMID29416129
OpenAlexW2786928529

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.