ReviewFrontiers in immunology2025
Stem cell activity shapes the pleiotropic effects of IFN-γ and TGF-β in autoimmune diseases, infections, and cancer, and drives autoimmune flares and remissions.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This work introduces stem cell activity as a central factor contributing to the pleiotropic effects of IFN-γ and TGF-β1, as well as to the fluctuations of autoimmune diseases (AIDs) between flares and remissions. Analysis of published data on hair follicle immune privilege indicates that immune protection is not an inherent feature of quiescent stem cells, as previously proposed, but instead depends on the specific pathways that regulate quiescence. While both IFN-γ and high levels of TGF-β1 induce stem cell quiescence, they exert opposite effects on immune privilege: IFN-γ upregulates MHC-I expression, whereas TGF-β1 downregulates it. Similar mechanisms apply to hematopoietic stem cell niches in the bone marrow. Moreover, cytokines such as IGF-1 and α-MSH, which enhance stem cell activity, also downregulate MHC-I. Different concentrations and combinations of these cytokines can promote or suppress stem cell activity and preserve or disrupt immune privilege, underscoring their multifaceted nature. Two mechanisms may contribute to the pleiotropic effects of IFN-γ and TGF-β1: opposing effects on bone marrow activity, with IFN-γ and high TGF-β1 acting in contrast, and differential effects of IFN-γ on immune attack intensity in the bone marrow versus the target tissue during AID. Stem cell dynamics also shape the course of AIDs: high stem cell activity supports tissue regeneration and remission, whereas quiescence together with tissue destruction by autoimmune attacks drives flares. A clear correlation emerges between the effects of various agents on stem cell activity and clinical outcomes in AIDs, highlighting the central role of stem cell activity in their pathogenesis. A proposed TGF-β1 gradient between protected stem cell reservoirs (hair follicle bulge, bone endosteal niches) and less protected regions enables simultaneous preservation of stem cells and regeneration of damaged tissue.
Indexed as
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.