Evidence map›Paper›PMID 41412962›Full record

ArticleAnnals of clinical and translational neurology2026

In-Depth Profiling Highlights the Effect of Efgartigimod on Peripheral Innate and Adaptive Immune Cells in Myasthenia Gravis.

Lei Jin, Liu Dong, Ying Wang, Dingxian He, Chong Yan, Jianying Xi, Haoqin Jiang, Yu Shi, Ming Guan, Chongbo Zhao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of clinical and translational neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Lei JinHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.
Liu DongDepartment of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Ying WangDepartment of Pharmacy, Huashan Hospital, Fudan University, Shanghai, China.
Dingxian HeHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.
Chong YanHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.
Jianying XiHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.ORCID 0000-0003-1028-3801
Haoqin JiangDepartment of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Yu ShiHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.
Ming GuanDepartment of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.
Chongbo ZhaoHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.
Jie SongHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.
Sushan LuoHuashan Rare Disease Centre and Department of Neurology, Huashan Hospital, Shanghai Medical College, National Centre for Neurological Disorders, Fudan University, Shanghai, China.ORCID 0000-0002-9033-7568

Funding

National Key Research and Development Program of China 2022YFC3501303National Key Research and Development Program of China 2022YFC3501305National Natural Science Foundation of China 82471426National Natural Science Foundation of China 82571592
6 · The paper itself

Abstract

backgroundMyasthenia gravis (MG) is an autoimmune disorder characterized by antibody-mediated complement activation. Efgartigimod, a neonatal Fc receptor (FcRn) antagonist, is approved for treating generalized MG (gMG). However, its modulatory effects on upstream innate and adaptive immune cells remain largely unexplored.

methodsWe first quantified FcRn expression in peripheral immune subsets from acetylcholine receptor antibodies (AChR-Ab) positive gMG. Then we assessed efgartigimod's impact on immune cells via in-depth profiling in vitro and later validated these findings in a prospective real-world cohort treated with efgartigimod.

resultsHigh FcRn expression was abundantly expressed on monocytes and lymphocytes in an exploratory MG cohort (n = 29), with notable intracellular presence. In vitro studies showed efgartigimod significantly decreased intracellular FcRn in monocytes (p < 0.001) and lymphocytes (p = 0.019). After efgartigimod treatment, non-classical monocytes (CD14

conclusionsBy integrating in vitro and clinical findings, we demonstrate that efgartigimod modulates peripheral immune cell populations, highlighting its significant immunomodulatory effects and clinical potential.

Indexed as

Adaptive ImmunityImmunity, InnateLymphocytesMonocytesMyasthenia GravisReceptors, FcAdultAgedFemaleHistocompatibility Antigens Class IHumansMaleMiddle AgedFc receptor, neonatalHistocompatibility Antigens Class IReceptors, FcEfgartigimodFcRngeneralized myasthenia gravisin‐depthperipheral immune cells

Identifiers

PMID41412962
PMCPMC13161891

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.