Evidence map›Paper›PMID 21157343›Full record

ReviewCurrent opinion in organ transplantation2011

Complement regulation of T-cell alloimmunity.

Hugo Raedler, Peter S Heeger

Abstract readReview
In one paragraph

Review in Current opinion in organ transplantation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. A novel injury site-natural antibody targeted complement inhibitor protects against lung transplant injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  2. Targeting the Complement Alternative Pathway Permits Graft Versus Leukemia Activity while Preventing Graft Versus Host Disease.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  3. Article
  4. Article
  5. Complement system in lung disease.American journal of respiratory cell and molecular biology · 2014
    Review
  6. Article
  7. CD46 in innate and adaptive immunity: an update.Clinical and experimental immunology · 2011
    Review
  8. 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

2 authors at 1 institution in 1 country.

Hugo RaedlerDepartment of Medicine, Recanati Miller Transplant Institute and Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.
Peter S Heeger
Icahn School of Medicine at Mount Sinai · US

Funding

Complement & T Cell Medicated Allograft RejectionR01AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2007 to 2016
$4.3M
GRAFT REJECTION AND DIRECT VERSUS INDIRECT RECOGNITIONR01AI043578 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 1998 to 2013
$3.8M
Complement & T Cell Medicated Allograft RejectionR56AI071185 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT · 2012 to 2012
$339k
NIAID NIH HHS AI071185NIAID NIH HHS AI43578NIAID NIH HHS R01 AI043578NIAID NIH HHS R01 AI071185NIAID NIH HHS R56 AI071185
6 · The paper itself

Abstract

purpose of reviewThe purpose of this review is to summarize recent findings implicating complement as an important regulator of T-cell immune responses. We then provide perspective for how these newly described mechanisms apply to allograft injury and how they could ultimately influence therapy. RECENT

findingsIn addition to known effects of serum complement as an effector arm of antibody-initiated injury, T cells and antigen-presenting cells produce complement proteins and up-regulate complement receptors following cognate interactions. The locally released and activated, immune cell-derived complement signals predominantly through C3a and C5a binding to their receptors expressed on both partners to induce immune cell activation and differentiation. Complement deficiency or blockade limits T-cell-mediated autoimmunity and transplant rejection, whereas removal of the complement regulatory protein decay accelerating factor can enhance T-cell immunity and accelerate graft rejection. SUMMARY: Emerging data indicate that immune cell-derived complement physiologically regulates immune cell survival and proliferation, modulating the strength and phenotype of adaptive T-cell immune responses involved in transplant rejection. The recognition of the diversity through which complement participates in allograft injury supports the need for continued design and testing of complement inhibitors in human transplant recipients.

Indexed as

Transplantation ImmunologyAnimalsAntigen-Presenting CellsAutoimmunityComplement System ProteinsGraft RejectionHumansT-LymphocytesComplement System Proteins

Identifiers

PMID21157343
PMCPMC3151543
OpenAlexW1964263868

What OpenQuestion holds

Textmetadata
LicenceTDM
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.