Evidence map›Paper›PMID 15277234›Full record

ArticleThe American journal of pathology2004

Loss of LFA-1, but not Mac-1, protects MRL/MpJ-Fas(lpr) mice from autoimmune disease.

Christopher G Kevil, M John Hicks, Xiaodong He, Junxuan Zhang, Christie M Ballantyne, Chander Raman, Trenton R Schoeb, Daniel C Bullard

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-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

40 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeting Neutrophil βBiomolecules · 2023
    Review
  4. Article
  5. CD11b agonists offer a novel approach for treating lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
  6. Immunogenetics of Lupus Erythematosus.Advances in experimental medicine and biology · 2022
    Article
  7. Immunosenescence: an unexplored role in glomerulonephritis.Clinical & translational immunology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mice expressing the variant rs1143679 allele of ITGAM (CD11b) show impaired DC-mediated T cell proliferation.Mammalian genome : official journal of the International Mammalian Genome Society · 2019
    Article
  15. Review
  16. Article
  17. 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

8 authors at 4 institutions in 1 country.

Christopher G KevilDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, LA, USA.
M John Hicks
Xiaodong He
Junxuan Zhang
Christie M Ballantyne
Chander Raman
Trenton R Schoeb
Daniel C Bullard
Pediatrics and Genetics · USBaylor College of Medicine · USLouisiana State University Health Sciences Center Shreveport · USUniversity of Alabama at Birmingham · US

Funding

IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
GENETIC MOUSE MODELS FOR CHRONIC INFLAMMATORY DISEASER01RR017009 · NCRR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BULLARD, DANIEL C · 2002 to 2006
$1.6M
CD5 REGULATION OF CK2 IN T CELLS OF DIFFERENT AGESR01AG016221 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAMAN, CHANDER · 1999 to 2004
$912k
NCRR NIH HHS R01 RR017009NCRR NIH HHS RR-017009NIAID NIH HHS T32 AI007051NIA NIH HHS R01 AG016221
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune complex-mediated tissue injury. Many different adhesion molecules are thought to participate in the development of SLE; however, few studies have directly examined the contributions of these proteins. Here we demonstrate that LFA-1 plays an essential role in the development of lupus in MRL/MpJ-Fas(lpr) mice. Mice deficient in LFA-1, but not Mac-1, showed significantly increased survival, decreased anti-DNA autoantibody formation, and reduced glomerulonephritis. The phenotype of the LFA-1-deficient mice was similar to that observed in beta(2) integrin-deficient (CD18-null) MRL/MpJ-Fas(lpr) mice, suggesting a lack of redundancy among the beta(2) integrin family members and other adhesion molecules. These studies identify LFA-1 as a key contributor in the pathogenesis of autoimmune disease in this model, and further suggest that therapeutic strategies targeting this adhesion molecule may be beneficial for the treatment of SLE.

Indexed as

AnimalsAutoantibodiesCD11 AntigensCD18 AntigensGlomerulonephritisKidney Function TestsLupus Erythematosus, SystemicLymphatic DiseasesLymphocyte Function-Associated Antigen-1Macrophage-1 AntigenMiceMice, Inbred C57BLMice, Inbred MRL lprMice, KnockoutAutoantibodiesCD11 AntigensCD18 AntigensLymphocyte Function-Associated Antigen-1Macrophage-1 Antigen

Identifiers

PMID15277234
PMCPMC1618580
OpenAlexW2129012249

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.