Evidence map›Paper›PMID 42812230›Full record

ArticleFrontiers in immunology2026

CX3CL1-CX3CR1 axis promotes restraint stress-induced thymic involution through macrophage-mediated thymocyte apoptosis.

Yuko Ishida, Yumi Kuninaka, Mizuho Nosaka, Akiko Ishigami, Naofumi Mukaida, Toshikazu Kondo

Abstract read
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

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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

6 authors.

Yuko IshidaDepartment of Forensic Medicine, Wakayama Medical University, Wakayama, Japan.
Yumi KuninakaDepartment of Forensic Medicine, Wakayama Medical University, Wakayama, Japan.
Mizuho NosakaDepartment of Forensic Medicine, Wakayama Medical University, Wakayama, Japan.
Akiko IshigamiDepartment of Forensic Medicine, Wakayama Medical University, Wakayama, Japan.
Naofumi MukaidaDepartment of Forensic Medicine, Wakayama Medical University, Wakayama, Japan.
Toshikazu KondoDepartment of Forensic Medicine, Wakayama Medical University, Wakayama, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Stress-induced thymic involution is characterized by rapid thymocyte loss and is largely attributed to glucocorticoid signaling. However, the local immune mechanisms involved remain unclear. We investigated the role of the CX3CL1-CX3CR1 axis in restraint stress (RS)-induced thymic involution. Methods: Wild-type (WT) and Results: RS increased CX3CL1 and CX3CR1 expression in thymic F4/80-positive macrophages. Conclusion: CX3CL1-CX3CR1 signaling contributes to RS-induced thymic involution through CX3CR1-dependent mechanisms involving macrophage-associated FasL-mediated thymocyte apoptosis and modulation of the corticosterone response, suggesting coordinated local immune and neuroendocrine mechanisms underlying stress-induced thymic involution.

Indexed as

ApoptosisChemokine CX3CL1CX3C Chemokine Receptor 1MacrophagesStress, PhysiologicalThymocytesThymus GlandAnimalsCorticosteroneFas Ligand ProteinMaleMiceMice, Inbred C57BLMice, KnockoutRestraint, PhysicalSignal TransductionChemokine CX3CL1CorticosteroneCX3C Chemokine Receptor 1Cx3cl1 protein, mouseCx3cr1 protein, mouseFas Ligand ProteinCX3CL1CX3CR1macrophagerestraint stressthymic involutionthymocyte apoptosis

Identifiers

PMID42812230
PMCPMC13619386

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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.