Evidence map›Paper›PMID 28393923›Full record

ReviewNature reviews. Immunology2017

Altered B cell signalling in autoimmunity.

David J Rawlings, Genita Metzler, Michelle Wray-Dutra, Shaun W Jackson

Abstract readReview
In one paragraph

Review in Nature reviews. Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 3 pooled it
10.1field-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

189 citing papers in PubMed, 3 syntheses or guidelines pooled it, 293 citations in OpenAlex.

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  17. Mechanisms of B Cell Tolerance in Health and Autoimmunity.Arthritis & rheumatology (Hoboken, N.J.) · 2026
    Review
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  20. Review

129 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 1 country.

David J RawlingsSeattle Children's Research Institute, 1900 9th Avenue, Seattle, Washington 98101, USA.
Genita MetzlerSeattle Children's Research Institute, 1900 9th Avenue, Seattle, Washington 98101, USA.
Michelle Wray-DutraSeattle Children's Research Institute, 1900 9th Avenue, Seattle, Washington 98101, USA.
Shaun W JacksonSeattle Children's Research Institute, 1900 9th Avenue, Seattle, Washington 98101, USA.
University of Washington · US

Funding

An integrated strategy to define the functional and synergistic impact of T1D causal variantsDP3DK111802 · NIDDK · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2016 to 2016
$4.4M
Defining the functional impact of T1D genes in mouse and man: a unified strategyDP3DK097672 · NIDDK · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2013
$4.4M
Lentiviral Gene Therapy for Wiskott-Aldrich SyndromeR01AI071163 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2008 to 2012
$3.5M
Lentiviral Gene Therapy of X-Linked AgammaglobulinemiaR01AI084457 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2012 to 2015
$2.5M
Basic Training at the Intersection of Innate and Adaptive Immunity in DiseaseT32AI106677 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL, GOVERMAN, JOAN M · 2013 to 2022
$2.1M
Lentiviral Gene Therapy of X-linked AgammaglobulinemiaR01HL075453 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2004 to 2008
$1.9M
B cell-intrinsic cytokine regulation and B cell-targeted therapies in murine lupuK08AI112993 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI JACKSON, SHAUN WILLIAM · 2014 to 2018
$910k
NHLBI NIH HHS R01 HL075453NIAID NIH HHS K08 AI112993NIAID NIH HHS R01 AI071163NIAID NIH HHS R01 AI084457NIAID NIH HHS T32 AI106677NIDDK NIH HHS DP3 DK097672NIDDK NIH HHS DP3 DK111802
6 · The paper itself

Abstract

Recent work has provided new insights into how altered B cell-intrinsic signals - through the B cell receptor (BCR) and key co-receptors - function together to promote the pathogenesis of autoimmunity. These combined signals affect B cells at two distinct stages: first, in the selection of the naive repertoire; and second, during extrafollicular or germinal centre activation responses. Thus, dysregulated signalling can lead to both an altered naive BCR repertoire and the generation of autoantibody-producing B cells. Strikingly, high-affinity autoantibodies predate and predict disease in several autoimmune disorders, including type 1 diabetes and systemic lupus erythematosus. This Review summarizes how, rather than being a downstream consequence of autoreactive T cell activation, dysregulated B cell signalling can function as a primary driver of many human autoimmune diseases.

Indexed as

AutoimmunityAnimalsB-LymphocytesHumansReceptors, Antigen, B-CellSignal TransductionReceptors, Antigen, B-Cell

Identifiers

PMID28393923
PMCPMC5523822
OpenAlexW2605871488

What OpenQuestion holds

Textmetadata
LicenceTDM
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.