Evidence map›Paper›PMID 42409961›Full record

ArticleExperimental & molecular medicine2026

Adipocyte OX40L promotes adipose T cell activation and insulin resistance in obesity.

Jianfeng Song, Qin Zeng, Yayi Jiao, Xiaoxiao Sun, Limin Xie, Jingpei Qiu, Yujin Ding, Wanyu Hu, Fanqi Wang, Biling Huang and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental & molecular medicine, 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

19 authors.

Jianfeng Song *National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Qin Zeng *National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Yayi Jiao *National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Xiaoxiao SunHenan Key Laboratory of Rare Diseases, Endocrinology and Metabolism Center, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Limin XieNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Jingpei QiuNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Yujin DingNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Wanyu HuNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Fanqi WangNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Biling HuangNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Wuqian MaiNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Ying MeiNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Dandan WangNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Lan XieTsinghua University, Intelligent Chinese Medicine Engineering Research Center, Beijing, 100084, China.
Xiang XiaoImmunobiology and Transplant Science Center and Department of Surgery, Houston Methodist Hospital, Houston, TX, USA.
Wei LiuDepartment of General Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China.
Willa A HsuehDiabetes and Metabolism Research Center, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, The Ohio State University, Columbus, OH, 43210, USA.
Xian C LiImmunobiology and Transplant Science Center and Department of Surgery, Houston Methodist Hospital, Houston, TX, USA.
Tuo DengNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, and Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. dengtuo@csu.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82130024National Natural Science Foundation of China (National Science Foundation of China) T2341005Natural Science Foundation of Hunan Province (Hunan Provincial Natural Science Foundation) 2023JJ40809
6 · The paper itself

Abstract

T cells contribute critically to obesity-induced adipose inflammation and insulin resistance, yet the co-stimulatory signals that govern their activation in adipose tissue remain unclear. Here, we systematically profile co-stimulatory molecules in adipocytes and adipose tissue macrophages and identify OX40 ligand (OX40L) as the most robustly upregulated in obesity. OX40L is also elevated in adipocytes from obese humans. Although macrophage-specific OX40L deletion has no metabolic impact, global OX40 deficiency or adipocyte-specific OX40L deletion reduces Th1 cell accumulation in visceral adipose tissue, attenuates inflammation and improves insulin sensitivity without affecting adiposity. These benefits are reversed by Th1 cell transfer. Therapeutic blockade of OX40L with a neutralizing antibody mimics the protective effects of genetic deletion. Our findings identify adipocyte-derived OX40L as a critical mediator of obesity-associated immune dysfunction and establish it as a targetable checkpoint for tissue-specific immunotherapy in metabolic disease.

Indexed as

AdipocytesAdipose TissueInsulin ResistanceLymphocyte ActivationObesityOX40 LigandT-LymphocytesAnimalsHumansMacrophagesMaleMiceOX40 Ligand

Identifiers

PMID42409961
PMCPMC13434776

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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.