Evidence map›Paper›PMID 34058061›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2021

C1q as a potential tolerogenic therapeutic in transplantation.

William M Baldwin, Anna Valujskikh, Robert L Fairchild

Open access · hybridAbstract read
In one paragraph

Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. C1q reprograms innate immune memory.Frontiers in immunology · 2025
    Article
  4. Article
  5. C1q and central nervous system disorders.Frontiers in immunology · 2023
    Review
  6. 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

3 authors at 1 institution in 1 country.

William M BaldwinInflammation and Immunity, Lerner Research Institute, Cleveland, Ohio, USA.ORCID 0000-0002-7271-1827
Anna ValujskikhInflammation and Immunity, Lerner Research Institute, Cleveland, Ohio, USA.ORCID 0000-0003-3252-0636
Robert L FairchildInflammation and Immunity, Lerner Research Institute, Cleveland, Ohio, USA.ORCID 0000-0002-7107-5259
Cleveland Clinic Lerner College of Medicine · US

Funding

Surgery CoreP01AI087586 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI VALUJSKIKH, ANNA · 2010 to 2019
$17.2M
NIAID NIH HHS P01 AI087586
6 · The paper itself

Abstract

In 1963, Lepow and colleagues resolved C1, the first component of the classical pathway, into three components, which they named C1q, C1r, and C1s. All three of these components were demonstrated to be involved in causing hemolysis in vitro. For over 30 years after that seminal discovery, the primary function attributed to C1q was as part of the C1 complex that initiated the classical pathway of the complement cascade. Then, a series of papers reported that isolated C1q could bind to apoptotic cells and facilitate their clearance by macrophages. Since then, rheumatologists have recognized that C1q is an important pattern recognition receptor (PRR) that diverts autoantigen containing extracellular vesicles from immune recognition. This critical function of C1q as a regulator of immune recognition has been largely overlooked in transplantation. Now that extracellular vesicles released from transplants have been identified as a major agent of immune recognition, it is logical to consider the potential impact of C1q on modulating the delivery of allogeneic extracellular vesicles to antigen presenting cells. This concept has clinical implications in the possible use of C1q or a derivative as a biological therapeutic to down-modulate immune responses to transplants.

Indexed as

Complement C1rComplement C1sComplement ActivationComplement C1qComplement C1qComplement C1rComplement C1santigen presentation/recognitionautoimmunitycell death: apoptosiscomplement biologyeditorial/personal viewpointimmunosuppression/immune modulationinnate immunity

Identifiers

PMID34058061
PMCPMC8564585
OpenAlexW3165368150

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.