Evidence map›Paper›PMID 23281837›Full record

ReviewArthritis research & therapy2012

B-cell selection and the development of autoantibodies.

Natalia V Giltiay, Craig P Chappell, Edward A Clark

Open access · goldAbstract readReview
In one paragraph

Review in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Review
  3. VDJ-REMIX: REpertoire Module Identification and eXploration.Bioinformatics (Oxford, England) · 2026
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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

3 authors at 1 institution in 1 country.

Natalia V GiltiayDepartment of Immunology, 1959 NE Pacific Street, University of Washington, Seattle, WA 98195, USA.
Craig P Chappell
Edward A Clark
University of Washington · US

Funding

Programming protective immunity by targeting antigens to the CD180 receptorR01AI052203 · NIAID · UNIVERSITY OF WASHINGTON · PI FULLER, DEBORAH H. · 2003 to 2019
$6.3M
FDRC1 AND FOLLICULAR DENDRITIC CELL SIGNALING PATHWAYSR37AI044257 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2004 to 2013
$4.0M
NIAID NIH HHS R01 AI052203NIAID NIH HHS R01AI52203NIAID NIH HHS R37 AI044257NIAID NIH HHS R37AI44257
6 · The paper itself

Abstract

The clearest evidence that B cells play an important role in human autoimmunity is that immunotherapies that deplete B cells are very effective treatments for many autoimmune diseases. All people, healthy or ill, have autoreactive B cells, but not at the same frequency. A number of genes influence the level of these autoreactive B cells and whether they are eliminated or not during development at a central checkpoint in the bone marrow (BM) or at a later checkpoint in peripheral lymphoid tissues. These genes include those encoding proteins that regulate signaling through the B-cell receptor complex such as Btk and PTPN22, proteins that regulate innate signaling via Toll-like receptors (TLRs) such as MyD88 and interleukin-1 receptor-associated kinase 4, as well as the gene encoding the activation-induced deaminase (AID) essential for B cells to undergo class switch recombination and somatic hypermutation. Recent studies have revealed that TLR signaling elements and AID function not only in peripheral B cells to help mediate effective antibody responses to foreign antigens, but also in the BM to help remove autoreactive B-lineage cells at a very early point in B-cell development. Newly arising B cells that leave the BM and enter the blood and splenic red pulp can express both AID and TLR signaling elements like TLR7, and thus are fully equipped to respond rapidly to antigens (including autoantigens), to isotype class switch, and to undergo somatic hypermutation. These red pulp B cells may thus be an important source of autoantibody-producing cells arising particularly in extrafollicular sites, and indeed may be as significant a source of autoantibody-producing cells as B cells arising from germinal centers.

Indexed as

AnimalsAutoantibodiesAutoantigensAutoimmunityB-LymphocytesGerminal CenterHumansImmunoglobulin Class SwitchingAutoantibodiesAutoantigens

Identifiers

PMID23281837
PMCPMC3535718
OpenAlexW2050564444

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.