Evidence map›Paper›PMID 41032891›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2025

Dynamic control of autoreactive B cells from spontaneous germinal centers.

Kristine Oleinika, Alexia Correia Ferreira, Selma Mouftakir, Carlos Castrillon, Lisa Madungwe, Usha Nair, Facundo D Batista, Michael C Carroll

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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

8 authors.

Kristine OleinikaProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.ORCID 0000-0002-2021-2938
Alexia Correia FerreiraProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.
Selma MouftakirProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.
Carlos CastrillonProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.
Lisa MadungweThe Ragon Institute of Mass General, MIT, and Harvard, Cambridge, MA, United States.
Usha NairThe Ragon Institute of Mass General, MIT, and Harvard, Cambridge, MA, United States.
Facundo D BatistaThe Ragon Institute of Mass General, MIT, and Harvard, Cambridge, MA, United States.ORCID 0000-0002-1130-9463
Michael C CarrollProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.ORCID 0000-0002-3213-4295

Funding

Evolution of autoreactive GC and epitope spreading in lupusR01AR074105 · NIAMS · BOSTON CHILDREN'S HOSPITAL · PI Michael Craig Carroll · 2018 to 2026
$4.2M
FDC regulation of self-reactive B cellsR01AI130307 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI CARROLL, MICHAEL CRAIG · 2018 to 2022
$2.7M
Lupus Research AllianceNIAID NIH HHS R01 AI130307NIAMS NIH HHS R01 AI130307NIAMS NIH HHS R01 AR074105NIH HHSU.S. Department of Defense HT9425-24-1-0598
6 · The paper itself

Abstract

Systemic lupus erythematosus is characterized by activation of many self-reactive B cell clones that produce autoantibodies. This can be modeled using mixed bone marrow chimeras, where autoreactive 564Igi B cells initiate autoimmunity that spreads to wild-type (WT) B cells. The mechanisms controlling the inclusion of new B cell clones into spontaneous germinal centers (GCs) remain unclear. Using CRISPR-Cas9, we generated 2 autoreactive B cell receptor knock-in strains, M05 and G55, based on B cell receptors from WT GC B cells in WT:564Igi chimeras. M05 and G55 mice lacked spontaneous GCs and overt autoantibody production, with receptor editing (λ light chain expression) contributing to tolerance. However, autoreactivity was not purged from the B cell compartment since presence of 564Igi clone allowed M05 and G55 B cells to join GCs and produce autoantibodies. These findings reveal that GCs can override peripheral tolerance, recruiting previously silent autoreactive clones and facilitating diversification of autoantibodies.

Indexed as

AutoimmunityB-LymphocytesGerminal CenterLupus Erythematosus, SystemicAnimalsAutoantibodiesGene Knock-In TechniquesImmune ToleranceMiceMice, Inbred C57BLReceptors, Antigen, B-CellAutoantibodiesReceptors, Antigen, B-CellautoantibodiesB cellsgerminal centersystemic lupus erythematosus (SLE)tolerance

Identifiers

PMID41032891
PMCPMC12726063

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Registered trials

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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.