ArticleResearch square2025
Foxp3
Article in Research square, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Endogenous Amphiregulin promotes muscle repair and function through expansion of fibro-adipogenic progenitors during chronicFrontiers in microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Inflammatory brain damage is an important factor contributing to mortality or lasting neurological sequelae in CNS infections, such as cryptococcal meningoencephalitis (CM), but little is known about natural immunoregulatory mechanisms in the infected brain. Here we report that regulatory T cells (Tregs) are a central immunoregulatory component in CM. Tregs are present within the CNS in both human CM patients and in the experimental murine CM. Treg-depletion exacerbates Th1-driven brain inflammation and neurological symptoms, accelerating mortality, despite enhanced fungal clearance in mouse CM. Aligned brain NanoString, scRNA-seq, and flow cytometry analyses revealed that Tregs reduce brain inflammation, especially T-cell recruitment activation and differentiation, shielding the brain from neurological damage. The major CNS-Treg recruitment appears to be chemokine receptor CCR8-mediated, supporting the importance of the CCR8/CCL1 axis in Treg recruitment into the brain. Tregs in CM are major producers of anti-inflammatory IL-10 and the growth factor Amphiregulin (Areg), which is implicated in neuronal repair. IL-10 deletion in murine CM phenocopies Treg depletion. Areg deletion showed no survival effect; however, IFN-γ production by effector T cells in the brain was reduced, supporting Aregs as a potential internal regulator of Treg immunosuppressive function. Finally, a Treg-enhancing immunotherapy using low dose IL-2-immune complex treatment substantially improves mouse survival and neurological outcomes. Together, we identified that Tregs are crucial for neuronal protection in CM, predominantly via IL-10 production, the CCR8-CCL1 axis is an important CNS-Treg recruitment mechanism and Treg enhancement is a potential therapeutic strategy to mitigate immunopathology during CM, and possibly other forms of meningitis.
Identifiers
What OpenQuestion holds
Registered trials
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.