Evidence map›Paper›PMID 37940849›Full record

ArticleBMC immunology2023

Increased infiltration of CD4

Toshihiko Nishioka, Kei-Ichi Katayama, Shinji Kumegawa, Kyoichi Isono, Takashi Baba, Hiroshi Tsujimoto, Gen Yamada, Norimitsu Inoue, Shinichi Asamura

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

9 authors at 1 institution in 1 country.

Toshihiko NishiokaDepartment of Plastic Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Kei-Ichi KatayamaDepartment of Molecular Genetics, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Shinji KumegawaDepartment of Plastic Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Kyoichi IsonoLaboratory Animal Center, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Takashi BabaDepartment of Molecular Genetics, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Hiroshi TsujimotoDepartment of Molecular Genetics, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Gen YamadaDepartment of Plastic Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Norimitsu InoueDepartment of Molecular Genetics, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan. inoue-no@wakayama-med.ac.jp.
Shinichi AsamuraDepartment of Plastic Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.
Wakayama Medical University · JP

Funding

Japan Society for the Promotion of Science JP21K09772
6 · The paper itself

Abstract

backgroundLymphedema is an intractable disease that can be caused by injury to lymphatic vessels, such as by surgical treatments for cancer. It can lead to impaired joint mobility in the extremities and reduced quality of life. Chronic inflammation due to infiltration of various immune cells in an area of lymphedema is thought to lead to local fibrosis, but the molecular pathogenesis of lymphedema remains unclear. Development of effective therapies requires elucidation of the immunological mechanisms involved in the progression of lymphedema. The complement system is part of the innate immune system which has a central role in the elimination of invading microbes and acts as a scavenger of altered host cells, such as apoptotic and necrotic cells and cellular debris. Complement-targeted therapies have recently been clinically applied to various diseases caused by complement overactivation. In this context, we aimed to determine whether complement activation is involved in the development of lymphedema.

resultsOur mouse tail lymphedema models showed increased expression of C3, and that the classical or lectin pathway was locally activated. Complement activation was suggested to be involved in the progression of lymphedema. In comparison of the C3 knockout (KO) mouse lymphedema model and wild-type mice, there was no difference in the degree of edema at three weeks postoperatively, but the C3 KO mice had a significant increase of TUNEL

conclusionsVigilance for exacerbation of lymphedema is necessary when surgical treatments have the potential to injure lymphatic vessels in patients undergoing complement-targeted therapies or with complement deficiency. Future studies should aim to elucidate the molecular mechanism of CD4

Indexed as

Lymphatic VesselsLymphedemaAnimalsCD4-Positive T-LymphocytesHumansInflammationMiceMice, Inbred C57BLMice, KnockoutQuality of LifeC3CD4+ T cellComplementDead cellsLymphedema

Identifiers

PMID37940849
PMCPMC10633916
OpenAlexW4388500859

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.