Evidence map›Paper›PMID 42292411›Full record

ArticleFrontiers in immunology2026

CXCL9 associates with experimental neuromyelitis optica spectrum disorder following adoptive transfer of Tfh and Th17 cells.

Liang Wang, Lei Zhou, Wenjuan Huang, Jingzi ZhangBao, Hongmei Tan, Yuxin Fan, Chuanzhen Lu, Jian Yu, Min Wang, Jiahong Lu and 3 more

Abstract read
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In one paragraph

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

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0citing papers in PubMed
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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

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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

13 authors.

Liang Wang *Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Lei Zhou *Department of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Wenjuan HuangDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Jingzi ZhangBaoDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Hongmei TanDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Yuxin FanDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Chuanzhen LuDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Jian YuDepartment of Ophthalmology and Vision Science, Eye and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Min WangDepartment of Ophthalmology and Vision Science, Eye and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Jiahong LuDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Chongbo ZhaoDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Jun WangDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Science, Shanghai Medical College, Shanghai Key Laboratory of Acupuncture Mechanism and Acupoint Function, Fudan University, Shanghai, China.
Chao QuanDepartment of Neurology and Rare Disease Center, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study investigates the pathogenic contributions of aquaporin-4 (AQP4)-specific follicular helper T (Tfh) and T helper 17 (Th17) cells in neuromyelitis optica spectrum disorder (NMOSD), utilizing newly established murine models based on adoptive transfer of antigen-specific T-cell populations. Methods: AQP4-knockout mice were immunized with the AQP4-derived peptide to generate AQP4-reactive Tfh and Th17 cells. These cells were subsequently isolated and adoptively transferred into wild-type recipient mice. At disease peak-defined by consistent neurological deficits-spinal cord and brain tissues were harvested for histopathological analysis, as well as immunohistochemistry. Central nervous system immune cell infiltration was quantified via flow cytometry. Total RNA was extracted from spinal cord tissue for bulk RNA sequencing; differentially expressed genes were validated using quantitative real-time PCR. Results: Recipient mice that received AQP4-reactive Tfh or Th17 cells developed progressive hind-limb weakness, with Th17-transferred mice exhibiting significantly more severe clinical scores. Histopathological analyses revealed robust perivascular inflammation, parenchymal immune infiltration, and focal demyelination. Immunohistochemical quantification demonstrated significantly increased the optical density of CD3, B220, GFAP, IBA1, and CXCL9, alongside markedly decreased MBP expression. Flow cytometric profiling confirmed substantial infiltration of leukocytes and activated microglia/macrophages into the central nervous system (CNS). Transcriptomic analysis identified CXCL9 as one of the most upregulated chemokines in the spinal cord; its astrocytic origin was further corroborated by confocal immunofluorescence co-localization with GFAP. Conclusion: Our findings establish that AQP4-specific Tfh and Th17 cells are sufficient to drive key neuropathological features of NMOSD-including microglial reactivity, leukocyte recruitment, neuroinflammation, and demyelination-

Indexed as

Adoptive TransferChemokine CXCL9Neuromyelitis OpticaT Follicular Helper CellsTh17 CellsAnimalsAquaporin 4Disease Models, AnimalFemaleMiceMice, Inbred C57BLMice, KnockoutSpinal CordAqp4 protein, mouseAquaporin 4Chemokine CXCL9aquaporin-4CXCL9follicular helper T cellneuromyelitis optica spectrum disorderT helper 17 cell

Identifiers

PMID42292411
PMCPMC13253477

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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.