Evidence map›Paper›PMID 36797799›Full record

ArticleInflammation and regeneration2023

A lesion-selective albumin-CTLA4Ig as a safe and effective treatment for collagen-induced arthritis.

Fu-Yao Jiang, Yan-Zhu Zhang, Yuan-Hong Tai, Chien-Yu Chou, Yu-Ching Hsieh, Ya-Chi Chang, Hsiao-Chen Huang, Zhi-Qin Li, Yuan-Chin Hsieh, I-Ju Chen and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation and regeneration, 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
1.5field-weighted citation impact, top 19% 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. Article
  2. Review
  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

19 authors at 4 institutions in 1 country.

Fu-Yao Jiang *Department of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Yan-Zhu Zhang *Department of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Yuan-Hong Tai *Institute of Molecular Medicine and Bioengineering, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Chien-Yu ChouInstitute of Molecular Medicine and Bioengineering, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Yu-Ching HsiehDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Ya-Chi ChangDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Hsiao-Chen HuangDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Zhi-Qin LiDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Yuan-Chin HsiehSchool of Medicine for International Students, I-Shou University, Kaoshiung, Taiwan, Republic of China.
I-Ju ChenSchool of Medicine, I-Shou University, Kaohsiung, Taiwan, Republic of China.
Bo-Cheng HuangInstitute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, Republic of China.
Yu-Cheng SuDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Wen-Wei LinDrug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China.
Hsin-Chieh LinDepartment of Materials Science and Engineering, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Jui-I ChaoDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Shyng-Shiou F YuanTranslational Research Center, Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, and Faculty and College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China.
Yun-Ming WangDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China.
Tian-Lu ChengDrug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of China.
Shey-Cherng TzouDepartment of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu, Taiwan, Republic of China. sctzou@nycu.edu.tw.ORCID http://orcid.org/0000-0002-6620-8571
National Yang Ming Chiao Tung University · TWKaohsiung Medical University · TWI-Shou University · TWNational Sun Yat-sen University · TW

Funding

Ministry of Science and Technology 107-2320-B-009-004Ministry of Science and Technology 109-2320-B-514 009-001Ministry of Science and Technology 110-2314-B-A49-003Ministry of Science and Technology 110-2320-B-A49-001National Yang Ming Chiao Tung University and Kaohsiung Medical University NCTUKMU109-517 DR-02National Yang Ming Chiao Tung University and Kaohsiung Medical University NYCUKMU-111-I002
6 · The paper itself

Abstract

backgroundCTLA4Ig is a dimeric fusion protein of the extracellular domain of cytotoxic T-lymphocyte protein 4 (CTLA4) and an Fc (Ig) fragment of human IgG

methodsWe linked albumin to the N-terminus of CTLA4Ig (termed Alb-CTLA4Ig) via a substrate sequence of matrix metalloproteinase (MMP). The binding activities and the biological activities of Alb-CTLA4Ig before and after MMP digestion were analyzed by a cell-based ELISA and an in vitro Jurkat T cell activation assay. The efficacy and safety of Alb-CTLA4Ig in treating joint inflammation were tested in mouse collagen-induced arthritis.

resultsAlb-CTLA4Ig is stable and inactive under physiological conditions but can be fully activated by MMPs. The binding activity of nondigested Alb-CTLA4Ig was at least 10,000-fold weaker than that of MMP-digested Alb-CTLA4Ig. Nondigested Alb-CTLA4Ig was unable to inhibit Jurkat T cell activation, whereas MMP-digested Alb-CTLA4Ig was as potent as conventional CTLA4Ig in inhibiting the T cells. Alb-CTLA4Ig was converted to CTLA4Ig in the inflamed joints to treat mouse collagen-induced arthritis, showing similar efficacy to that of conventional CTLA4Ig. In contrast to conventional CTLA4Ig, Alb-CTLA4Ig did not inhibit the antimicrobial responses in the spleens of the treated mice.

conclusionsOur study indicates that Alb-CTLA4Ig can be activated by MMPs to suppress tissue inflammation in situ. Thus, Alb-CTLA4Ig is a safe and effective treatment for collagen-induced arthritis in mice.

Indexed as

Adverse effectsAlbuminCollagen-induced arthritisCTLA4IgInflammatory lesion-selectiveMatrix metalloproteinase (MMP)Protein engineering

Identifiers

PMID36797799
PMCPMC9933273
OpenAlexW4321095288

What OpenQuestion holds

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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.