Evidence map›Paper›PMID 38828725›Full record

ArticleThe Journal of clinical investigation2024

Hexamerization: explaining the original sin of IgG-mediated complement activation in acute lung injury.

Hrishikesh S Kulkarni

Abstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Hrishikesh S Kulkarni

Funding

Lung epithelial cell-derived C3 in acute lung injuryR01HL169860 · NHLBI · WASHINGTON UNIVERSITY · PI Hrishikesh Satish Kulkarni · 2023 to 2026
$2.3M
Lung-derived complement in pneumoniaR01HL166449 · NHLBI · WASHINGTON UNIVERSITY · PI Hrishikesh Satish Kulkarni · 2023 to 2026
$2.2M
C3 Mitigates Epithelial Injury in PneumoniaK08HL148510 · NHLBI · WASHINGTON UNIVERSITY · PI KULKARNI, HRISHIKESH SATISH · 2019 to 2023
$740k
NHLBI NIH HHS K08 HL148510NHLBI NIH HHS R01 HL166449NHLBI NIH HHS R01 HL169860
6 · The paper itself

Abstract

Although antibody-mediated lung damage is a major factor in transfusion-related acute lung injury (ALI), autoimmune lung disease (for example, coatomer subunit α [COPA] syndrome), and primary graft dysfunction following lung transplantation, the mechanism by which antigen-antibody complexes activate complement to induce lung damage remains unclear. In this issue of the JCI, Cleary and colleagues utilized several approaches to demonstrate that IgG forms hexamers with MHC class I alloantibodies. This hexamerization served as a key pathophysiological mechanism in alloimmune lung injury models and was mediated through the classical pathway of complement activation. Additionally, the authors provided avenues for exploring therapeutics for this currently hard-to-treat clinical entity that has several etiologies but a potentially focused mechanism.

Indexed as

Acute Lung InjuryComplement ActivationImmunoglobulin GAnimalsAntigen-Antibody ComplexHistocompatibility Antigens Class IHumansIsoantibodiesProtein MultimerizationAntigen-Antibody ComplexHistocompatibility Antigens Class IImmunoglobulin GIsoantibodies

Identifiers

PMID38828725
PMCPMC11142731

What Socratic holds

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Registered trials

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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 Socratic graph.