Evidence map›Paper›PMID 37978415›Full record

ArticleArthritis research & therapy2023

TIGIT reverses IFN-α-promoted Th1-like Tregs via in-sequence effects dependent on STAT4.

Shihan Yu, Jia Gu, Rui Wang, Seunghyun Lee, Yu Shan, Jiakai Wang, Yini Sun, Xiaoxue Ma

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

Article in Arthritis research & therapy, 2023. 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
1.2field-weighted citation impact, top 20% 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, 7 citations in OpenAlex.

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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

8 authors at 5 institutions in 3 countries.

Shihan Yu *Department of Pediatrics, The First Hospital of China Medical University, No.155, Nanjingbei Street, Heping District, Shenyang, 110001, China.
Jia Gu *Department of Pediatrics, The First Hospital of China Medical University, No.155, Nanjingbei Street, Heping District, Shenyang, 110001, China.
Rui Wang *Department of Pediatrics, The First Hospital of China Medical University, No.155, Nanjingbei Street, Heping District, Shenyang, 110001, China.
Seunghyun LeeDepartment of Preventive Medicine, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Yu ShanDepartment of Pediatrics, Shenyang Women's and Children's Hospital, Shenyang, China.
Jiakai WangDepartment of Rheumatology and Immunology, The First Hospital of China Medical University, Shenyang, China.
Yini SunDepartment of Critical Care Medicine, The First Hospital of China Medical University, Shenyang, China.
Xiaoxue MaDepartment of Pediatrics, The First Hospital of China Medical University, No.155, Nanjingbei Street, Heping District, Shenyang, 110001, China. snow1999521@126.com.
First Hospital of China Medical University · CNChina Medical University · CNChung-Ang University · KRShenyang First People's Hospital · CNXinHua Hospital · CN

Funding

Liaoning Province Natural Science Foundation 2022-BS-134National Natural Science Foundation of China 81901658National Natural Science Foundation of China 82102266
6 · The paper itself

Abstract

objectivesThe induction direction of interferon (IFN)-α in T-cell phenotype and function varies depending on the activation state of the cell and the time of stimulation. To assess the effects of elevated IFN-α on regulatory T cells (Tregs) in systemic lupus erythematosus (SLE) patients, we investigated the differentiation of Th1-like Tregs under in-sequence and out-of-sequence conditions and the reversal effect of activating TIGIT on immune suppression.

methodsPhenotypes and activation levels of Tregs from SLE patients and healthy controls were analyzed using flow cytometry. In vitro culture conditions based on the sequence of TCR activation and IFN-α stimulation simulated in-sequence or out-of-sequence effects. CD4

resultsThe frequency of Th1-like Tregs and activation levels of Tregs increased, but TIGIT expression in Tregs decreased in SLE patients. IFN-α promoted the conversation of Tregs to Th1-like Tregs while reducing immunosuppressive function under in-sequence conditions. The STAT4 pathway, but not the STAT1 pathway, was crucial for the IFN-α-mediated in-sequence effects. Reactivation of TIGIT reversed Th1 polarization of Tregs by suppressing AKT/mTOR and STAT4 signaling.

conclusionsOur findings suggest that IFN-α mediated in-sequence effects on Tregs may be responsible for the expansion of Th1-like Tregs in SLE. TIGIT can restore immune suppression damage in Tregs and represents a potential therapeutic target for SLE.

Indexed as

Lupus Erythematosus, SystemicProto-Oncogene Proteins c-aktHumansInterferon-alphaReceptors, ImmunologicSTAT4 Transcription FactorT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesInterferon-alphaProto-Oncogene Proteins c-aktReceptors, ImmunologicSTAT4 protein, humanSTAT4 Transcription FactorTIGIT protein, humanTOR Serine-Threonine KinasesIFN-αSequence effectSLETh1-like TregTIGIT

Identifiers

PMID37978415
PMCPMC10655484
OpenAlexW4388769300

What OpenQuestion 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 OpenQuestion graph.