Evidence map›Paper›PMID 10359584›Full record

ArticleThe Journal of experimental medicine1999

MRL-lpr/lpr mice exhibit a defect in maintaining developmental arrest and follicular exclusion of anti-double-stranded DNA B cells.

L Mandik-Nayak, S J Seo, C Sokol, K M Potts, A Bui, J Erikson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

54 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. Article
  3. γδ T cells in immune-mediated kidney disease.European journal of immunology · 2024
    Review
  4. Article
  5. T cell help in the autoreactive germinal center.Scandinavian journal of immunology · 2022
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Loss of an IgG plasma cell checkpoint in patients with lupus.The Journal of allergy and clinical immunology · 2019
    Article
  11. Review
  12. Article
  13. Anti-Insulin B Cells Are Poised for Antigen Presentation in Type 1 Diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Loss of Immune Tolerance Is Controlled by ICOS in Sle1 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  19. IDO2: A Pathogenic Mediator of Inflammatory Autoimmunity.Clinical medicine insights. Pathology · 2016
    Review
  20. 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

6 authors at 1 institution in 1 country.

L Mandik-NayakThe Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
S J Seo
C Sokol
K M Potts
A Bui
J Erikson
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007170 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BRASS, LAWRENCE F · 1985 to 2022
$54.0M
TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
TRANSGENIC MODEL FOR B CELL TOLERANCE AND AUTOIMMUNITYR01AI032137 · NIAID · WISTAR INSTITUTE · PI ERIKSON, JAN S. · 1997 to 2009
$4.3M
NCI NIH HHS CA-09171NCI NIH HHS CA10815NCI NIH HHS P30 CA010815NCI NIH HHS T32 CA009171NIAID NIH HHS 5R01 AI32137-06NIAID NIH HHS R01 AI032137NIGMS NIH HHS T32 GM007170
6 · The paper itself

Abstract

A hallmark of systemic lupus erythematosus and the MRL murine model for lupus is the presence of anti-double-stranded (ds)DNA antibodies (Abs). To identify the steps leading to the production of these Abs in autoimmune mice, we have compared the phenotype and localization of anti-dsDNA B cells in autoimmune (MRL+/+ and lpr/lpr) mice with that in nonautoimmune (BALB/c) mice. Anti-dsDNA B cells are actively regulated in BALB/c mice as indicated by their developmental arrest and accumulation at the T-B interface of the splenic follicle. In the MRL genetic background, anti-dsDNA B cells are no longer developmentally arrested, suggesting an intrinsic B cell defect conferred by MRL background genes. With intact Fas, they continue to exhibit follicular exclusion; however, in the presence of the lpr/lpr mutation, anti-dsDNA B cells are now present in the follicle. Coincident with the altered localization of anti-dsDNA B cells is a follicular infiltration of CD4 T cells. Together, these data suggest that MRL mice are defective in maintaining the developmental arrest of autoreactive B cells and indicate a role for Fas in restricting entry into the follicle.

Indexed as

AnimalsAntibodies, AntinuclearAntigens, CDAutoimmunityB-LymphocytesCD4-Positive T-LymphocytesCell Differentiationfas ReceptorLupus Erythematosus, SystemicMiceMice, Inbred BALB CMice, Inbred MRL lprMice, TransgenicAntibodies, AntinuclearAntigens, CDfas Receptor

Identifiers

PMID10359584
PMCPMC2193088
OpenAlexW2099958255

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.