Evidence map›Paper›PMID 41316274›Full record

ArticleCell communication and signaling : CCS2025

The interplay between M2-like macrophages and Th17.1 cells promotes the progression of early-stage sarcoidosis.

Yu Zhao, Xiujuan Zhang, Liang Dong, Ning Zhu, Daibing Zhou, Shuanghui Li, Junzhu Lv, Gulinuer Wumaier, Jing Wang, Yuzhen Zeng and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. New Therapies for Sarcoidosis: Molecular and Pathophysiological Basis.International journal of molecular sciences · 2026
    Review
  2. 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

17 authors.

Yu Zhao *Department of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Xiujuan Zhang *Department of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Liang DongDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Ning ZhuDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Daibing ZhouDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Shuanghui LiDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Junzhu LvDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Gulinuer WumaierDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Jing WangDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Yuzhen ZengDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Weiyuan FangDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Wanfeng XiongDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Chengwei LiDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Mengqi XuDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
An CuiDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Ruzetuoheti YiminniyazeDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China.
Shengqing LiDepartment of Pulmonary and Critical Care Medicine, Huashan Hospital, Fudan University, No.12 Urumqi Middle Road, Shanghai, China. shengqing_li@fudan.edu.cn.

Funding

National Natural Science Foundation of China No. 82270058, No. 82241028National Natural Science Foundation of China No82400077Shanghai Year 2022 Science and Technology Innovation Action Plan Medical Innovation Research Special Project No. 22Y11900600
6 · The paper itself

Abstract

backgroundSarcoidosis is pathologically characterized by non-necrotizing granulomas inflammation. Despite the high spontaneous remission rate, a remarkable number of sarcoidosis patients undergo persistent progression. Glucocorticoids are currently recommended as the first-line treatment for sarcoidosis, but the therapeutic responses showed a great heterogeneity in clinical practice. We investigated the role of macrophages and Th17.1 cells in the poor response to glucocorticoid and progression in the early-stage sarcoidosis. METHODS AND MAIN

resultsCyTOF was performed on the mediastinal lymph nodes and peripheral blood samples to probe the alterations of immune cells in sarcoidosis. Monocytes were enriched in sarcoidosis patients but with impaired functions of antigen processing and presentation. Meanwhile, Th17.1 cells were enriched and overactivated in sarcoidosis. Both macrophages and Th17.1 cells were recruited to the granuloma lesions by CCL2 and CXCL-9/10, respectively. The granulomas of sarcoidosis in lymph nodes were classified as 3 types: M1-like macrophage-dominated type (type I), M1/2-mixed macrophage type (type II) and M2-like macrophage-dominated type (type III). Type III granuloma with elevated Th17.1 cells and M2-like macrophages predict a poor therapeutic response of sarcoidosis patients. In addition, Th17.1 cells impaired the antigen phagocytic and processing ability of macrophages through CD47/SIRPα interaction. Blockade of CD47/SIRPα interaction significantly repressed the progression of sarcoidosis in mouse model.

conclusionsOur study reveals a novel interaction between Th17.1 cells and M2-like macrophages in Type III granulomas potentially mediated through CD47-SIRPα, which may contribute to impaired antigen processing and glucocorticoid resistance in sarcoidosis. Therapies targeting this molecular pathway represent a promising direction for developing new sarcoidosis treatments.

Indexed as

Disease ProgressionMacrophagesSarcoidosisTh17 CellsAdultAnimalsFemaleGranulomaHumansLymph NodesMaleMiceMiddle AgedCD47M2 macrophageSarcoidosisSIRPαTh17.1 cell

Identifiers

PMID41316274
PMCPMC12763982

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.