Evidence map›Paper›PMID 17950717›Full record

ReviewCellular immunology2007

New concepts of complement in allorecognition and graft rejection.

Barbara A Wasowska, Chih-Yuan Lee, Marc K Halushka, William M Baldwin

Open access · greenAbstract readReview
In one paragraph

Review in Cellular immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Memory B cells in transplantation.Transplantation · 2015
    Review
  9. Article
  10. Review
  11. Article
  12. Chronic alloantibody mediated rejection.Seminars in immunology · 2012
    Review
  13. A novel method of measuring cardiac preservation injury demonstrates University of Wisconsin solution is associated with less ischemic necrosis than Celsior in early cardiac allograft biopsy specimens.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2012
    Article
  14. Article
  15. Characterization of immune responses to cardiac self-antigens myosin and vimentin in human cardiac allograft recipients with antibody-mediated rejection and cardiac allograft vasculopathy.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2010
    Article
  16. Article
  17. Review
  18. New concepts in alloimmune recognition.Cellular immunology · 2007
    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

4 authors at 1 institution in 1 country.

Barbara A WasowskaThe Department of Pathology, Ross Research Building, Room 659, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205-2196, USA.
Chih-Yuan Lee
Marc K Halushka
William M Baldwin
Johns Hopkins University · US

Funding

Stat3 in Post-Ischemic Myocardial InflammationP01HL065608 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, LEWIS C · 2000 to 2011
$22.0M
Role of the Granzyme B Pathway in AGAP01HL056091 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BALDWIN, WILLIAM M · 1997 to 2007
$10.9M
COMPLEMENT MEDIATED INJURY IN ALLOGRAFT REJECTIONR01AI042387 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BALDWIN, WILLIAM M · 1997 to 2007
$3.1M
NHLBI NIH HHS P01 HL056091NHLBI NIH HHS P01 HL065608NHLBI NIH HHS P01 HL56091NHLBI NIH HHS P01 HL65608NIAID NIH HHS R01 AI042387NIAID NIH HHS R01AI42387
6 · The paper itself

Abstract

In transplantation, activation of complement has largely been equated to antibody-mediated rejection, but complement is also important in recognition of apoptotic and necrotic cells as well as in modifying antigen presentation to T cells and B cells. As a part of the innate immune system, complement is one of the first responses to injury, and it can determine the direction and magnitude of the subsequent responses. Consequently, the effects of complement in allorecognition and graft rejection are increased when organs are procured from cadaver donors because these organs sustain a series of stresses from brain death, prolonged life support, ischemia and finally reperfusion that initiate proinflammatory processes and tissue injury. In addition, these organs are transplanted to patients, who frequently have been sensitized to histocompatibility antigens as the result of transfusions, pregnancies or transplants. Complement activation generates a series of biologically active effector molecules that can modulate graft rejection by directly binding to the graft or by modifying the response of macrophages, T and B cells of the recipient. However, complement is regulated and the process of regulation produces split products that can decrease as well as increase immune responses. Small animal models have been developed to test these variables. The guide for evaluating results from these models remains clinical findings because there are significant differences between the rodent and human complement systems.

Indexed as

Complement ActivationComplement System ProteinsAnimalsAntigen PresentationB-LymphocytesCadaverComplement Pathway, AlternativeComplement Pathway, ClassicalFemaleGraft RejectionHeart TransplantationHumansIsoantigensModels, AnimalPregnancyReperfusion InjuryComplement System ProteinsIsoantigens

Identifiers

PMID17950717
PMCPMC2139895
OpenAlexW2058364976

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.