Evidence map›Paper›PMID 20584999›Full record

ArticleDiabetes2010

Immune cell-derived c3 is required for autoimmune diabetes induced by multiple low doses of streptozotocin.

Marvin Lin, Na Yin, Barbara Murphy, M Edward Medof, Stephan Segerer, Peter S Heeger, Bernd Schröppel

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Intracellular C3 protects β-cells from IL-1β-driven cytotoxicity via interaction with Fyn-related kinase.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Annals of nuclear medicine · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Absence of recipient C3aR1 signaling limits expansion and differentiation of alloreactive CD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
    Article
  10. C5aR1 regulates migration of suppressive myeloid cells required for costimulatory blockade-induced murine allograft survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
    Article
  11. Article
  12. T Cell Expression of C5a Receptor 2 Augments Murine Regulatory T Cell (TJournal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Complement regulation of T-cell alloimmunity.Seminars in nephrology · 2013
    Review
  18. Immune cell-derived C3a and C5a costimulate human T cell alloimmunity.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2013
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Marvin LinDivision of Nephrology, Mount Sinai School of Medicine, New York, New York, USA.
Na Yin
Barbara Murphy
M Edward Medof
Stephan Segerer
Peter S Heeger
Bernd Schröppel
Icahn School of Medicine at Mount Sinai · USCase Western Reserve University · USUniversity Hospital of Zurich · CH

Funding

Complement & T Cell Medicated Allograft RejectionR01AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2007 to 2016
$4.3M
PROTECTION OF THE OCULAR SURFACER01EY011288 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MEDOF, MELVIN EDWARD · 1996 to 2006
$1.5M
Contribution of Toll-like receptor signaling in islet transplantationK08AI071038 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SCHROPPEL, BERND · 2007 to 2010
$618k
Complement & T Cell Medicated Allograft RejectionR56AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2012 to 2012
$339k
NEI NIH HHS EY105476NEI NIH HHS EY11288NEI NIH HHS R01 EY011288NIAID NIH HHS AI-071185NIAID NIH HHS K08 AI071038NIAID NIH HHS KO8 AI 071038NIAID NIH HHS R01 AI071185NIAID NIH HHS R56 AI071185
6 · The paper itself

Abstract

objectiveThe complement system contributes to autoimmune injury, but its involvement in promoting the development of autoimmune diabetes is unknown. In this study, our goal was to ascertain the role of complement C3 in autoimmune diabetes. RESEARCH DESIGN AND

methodsSusceptibility to diabetes development after multiple low-dose streptozotocin treatment in wild-type (WT) and C3-deficient mice was analyzed. Bone marrow chimeras, luminex, and quantitative reverse transcription PCR assays were performed to evaluate the phenotypic and immunologic impact of C3 in the development of this diabetes model.

resultsCoincident with the induced elevations in blood glucose levels, we documented alternative pathway complement component gene expression within the islets of the diabetic WT mice. When we repeated the experiments with C3-deficient mice, we observed complete resistance to disease, as assessed by the absence of histologic insulitis and the absence of T-cell reactivity to islet antigens. Studies of WT chimeras bearing C3-deficient bone marrow cells showed that bone marrow cell-derived C3, and not serum C3, is involved in the induction of diabetes in this model.

conclusionsThe data reveal a key role for immune cell-derived C3 in the pathogenesis of murine multiple low-dose streptozotocin-induced diabetes and support the concept that immune cell mediated diabetes is in part complement-dependent.

Indexed as

AnimalsBlood GlucoseBone Marrow CellsComplement C3Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Genetic Predisposition to DiseaseIslets of Langerhans TransplantationLymphocyte ActivationMaleMiceMice, KnockoutPolymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionStreptozocinT-LymphocytesBlood GlucoseComplement C3Streptozocin

Identifiers

PMID20584999
PMCPMC2927947
OpenAlexW2052502118

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.