Evidence map›Paper›PMID 12213736›Full record

ArticleThe American journal of pathology2002

Deletion of decay-accelerating factor (CD55) exacerbates autoimmune disease development in MRL/lpr mice.

Takashi Miwa, Michael A Maldonado, Lin Zhou, Xiujun Sun, Hong Yuan Luo, Dewei Cai, Victoria P Werth, Michael P Madaio, Robert A Eisenberg, Wen-Chao Song

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

46 citing papers in PubMed, 95 citations in OpenAlex.

  1. Immune regulation by CD55 in chronic beryllium disease.American journal of respiratory cell and molecular biology · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. CD8Nature communications · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Complement in Lupus Nephritis: New Perspectives.Kidney diseases (Basel, Switzerland) · 2015
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice.Journal of immunology (Baltimore, Md. : 1950) · 2012
    Article
  18. Article
  19. Article
  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

10 authors at 3 institutions in 1 country.

Takashi MiwaDepartment of Pharmacology, Center for Experimental Therapeutics, Philadelphia, Pennsylvania, USA.
Michael A Maldonado
Lin Zhou
Xiujun Sun
Hong Yuan Luo
Dewei Cai
Victoria P Werth
Michael P Madaio
Robert A Eisenberg
Wen-Chao Song
Center for Rheumatology · USIo Therapeutics (United States) · USUniversity of Pennsylvania · US

Funding

BIOLOGY OF DECAY ACCELERATING FACTORR01AI044970 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2000 to 2014
$4.9M
NIAID NIH HHS AI 44970NIAID NIH HHS R01 AI044970
6 · The paper itself

Abstract

Decay-accelerating factor (DAF, CD55) is a glycosylphosphatidylinositol-anchored membrane protein that restricts complement activation on autologous cells. It is also a ligand for CD97, an activation-associated lymphocyte antigen with seven transmembrane domains. It is widely expressed on cells of both the hematopoietic and nonhematopoietic lineages. Although deficiency of DAF on human erythrocytes is associated with the hemolytic anemia syndrome paroxysmal nocturnal hemoglobinuria, the in vivo biology of DAF is still poorly understood. We addressed the in vivo function of DAF in a knockout mouse model and describe here that deletion of DAF exacerbates autoimmune disease development in MRL/lpr mice, a model for human systemic lupus erythematosus. Compared to DAF-sufficient littermate controls, DAF-deficient female MRL/lpr mice developed exacerbated lymphadenopathy and splenomegaly, higher serum anti-chromatin autoantibody levels, and aggravated dermatitis. Consistent with the phenotype of aggravated dermatitis in DAF-deficient mice, Northern and Western blots and immunofluorescence studies showed DAF to be expressed abundantly in the mouse skin, suggesting that it may play a particularly important role in this tissue. Histology and immunostaining demonstrated inflammatory infiltrate and focal C3 deposition in early skin lesions, mostly along the dermal-epidermal junction. These results reveal a protective function of DAF in the development of a systemic autoimmune syndrome and suggest that dysfunction or down-regulation of DAF may contribute to autoimmune disease pathogenesis and manifestation.

Indexed as

Disease Models, AnimalAnimalsCD55 AntigensFemaleGene DeletionHumansLupus Erythematosus, SystemicMiceMice, KnockoutCD55 Antigens

Identifiers

PMID12213736
PMCPMC1867258
OpenAlexW2135382699

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.