Evidence map›Paper›PMID 42218289›Full record

ArticleScientific reports2026

Anti-human T lymphocyte porcine immunoglobulin attenuates experimental autoimmune encephalomyelitis by inhibiting T cell activation.

Junchen Liu, Xilin Nie, Fan Yang, Peng Geng, Jingwen Jin, Xuan Liu, Lingchen Kong, Yipeng Zhao, Wenqian Mao, Qianwen Ma and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

22 authors.

Junchen Liu *Department of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Xilin Nie *Department of Research and Development, Wuhan Institute of Biological Products, Wuhan, China.
Fan Yang *Department of Research and Development, Wuhan Institute of Biological Products, Wuhan, China.
Peng GengDepartment of Research and Development, Wuhan Institute of Biological Products, Wuhan, China.
Jingwen JinDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Xuan LiuDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Lingchen KongDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Yipeng ZhaoDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Wenqian MaoDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Qianwen MaDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Yinghao SongDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Jiaxuan WuDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Ruizhu WangDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Taoxiang ChenSchool of Basic Medical Sciences-Weifang Joint Research Center for Pediatric Neurological Diseases and Innovation and Transformation, Wuhan University, Wuhan, China.
Biwen PengSchool of Basic Medical Sciences-Weifang Joint Research Center for Pediatric Neurological Diseases and Innovation and Transformation, Wuhan University, Wuhan, China.
Wanhong LiuDepartment of Immunology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Jian XuSchool of Basic Medical Sciences-Weifang Joint Research Center for Pediatric Neurological Diseases and Innovation and Transformation, Wuhan University, Wuhan, China.
Yuanteng FanSchool of Basic Medical Sciences-Weifang Joint Research Center for Pediatric Neurological Diseases and Innovation and Transformation, Wuhan University, Wuhan, China.
Jun YinDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Zhi ZhangDepartment of Research and Development, Wuhan Institute of Biological Products, Wuhan, China. 13995672848@139.com.
Song HanDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China. hansong@whu.edu.cn.
XiaoHua HeDepartment of Pathophysiology, Taikang Medical School, School of Basic Medical Sciences, Wuhan University, Wuhan, China.

Funding

Department of Science and Technology of Hubei Province 2017CFA017Department of Science and Technology of Hubei Province 2017CFB698Wuhan Municipal Science and Technology Bureau 2022020801020489Wuhan University TFLC2018001Wuhan University ZNLH201909
6 · The paper itself

Abstract

Anti-human T lymphocyte porcine immunoglobulin (P-ATG) is a type of anti-thymocyte globulin (ATG) drug that has been used as an immunosuppressant for severe aplastic anemia and graft-versus-host disease for decades. However, the potential application of ATG for the direct treatment of Multiple sclerosis (MS) and the immune regulatory mechanisms are still unclear. In this study, the therapeutic effects and possible underlying mechanisms of P-ATG were evaluated in the rat model of experimental autoimmune encephalomyelitis (EAE), the animal model of MS. P-ATG could bind to T cells in both human and rat PBMCs in vitro and inhibit inflammatory cytokines secretion from stimulated T cells. P-ATG treatment effectively ameliorated behavioral and pathological alterations in EAE rats through reducing inflammatory infiltration and demyelination in the spinal cords. Moreover, P-ATG treatment significantly suppressed the immune response of T cells, as indicated by a decrease in the IFN-γ

Indexed as

Antilymphocyte SerumEncephalomyelitis, Autoimmune, ExperimentalLymphocyte ActivationT-LymphocytesAnimalsCytokinesDisease Models, AnimalFemaleHumansRatsSwineTh17 CellsTh1 CellsAntilymphocyte SerumCytokinesAnti-human T lymphocyte porcine immunoglobulinExperimental autoimmune encephalomyelitisMultiple sclerosisTh17 cellsTh1 cells

Identifiers

PMID42218289
PMCPMC13458704

What Socratic 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 Socratic graph.