# Immune cytokines as a bridge linking the gut–liver–ovary axis in the pathogenesis of premature ovarian failure

**Authors:** Huimin Xu, Muxi Li, Shouyan Yang, Deyou Jiang

PMC · DOI: 10.3389/fendo.2026.1758707 · Frontiers in Endocrinology · 2026-03-04

## TL;DR

This paper explores how immune cytokines connect gut health, liver function, and ovarian failure, offering new insights into the causes and treatment of premature ovarian failure.

## Contribution

The paper introduces a novel conceptual framework linking immune cytokines to the gut-liver-ovary axis in premature ovarian failure.

## Key findings

- Immune cytokines act as a central hub connecting gut microbiota dysbiosis, bile acid metabolism, and premature ovarian failure.
- Regulatory T cells, interferon-γ, and Th17 cells are key immune mediators in the pathogenesis of POF.
- The gut-liver-ovary axis is closely linked to immune-related pathways in POF progression.

## Abstract

Premature ovarian failure (POF) is a multifactorial disorder characterized by the progressive decline of ovarian function, in which autoimmune factors account for approximately 10%–30% of cases. Accumulating evidence has demonstrated that immune-related mediators, including regulatory T cells (Tregs), interferon-γ (IFN-γ), and T helper 17 (Th17) cells, play pivotal regulatory roles in its initiation and progression. In recent years, the gut–liver axis and its potential mechanistic links with POF have emerged as a research hotspot in this field. Notably, these pathways are closely associated with the expression and functional balance of key immune mediators such as Tregs, IFN-γ, and Th17 cells. Based on the bridging role of immune cytokines between POF and the gut–liver axis, we propose a novel conceptual framework in which immune cytokines serve as a central hub to systematically elucidate the intrinsic connections among POF, gut microbiota dysbiosis, and bile acid metabolism. Furthermore, we highlight the current limitations of existing studies in this area. This perspective may provide a new theoretical framework for understanding the pathogenesis of POF and holds significant scientific value. Importantly, it may also offer novel insights and potential evidence for expanding clinical diagnostic and therapeutic strategies.

## Linked entities

- **Diseases:** premature ovarian failure (MONDO:0001119)

## Full-text entities

- **Genes:** IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}
- **Diseases:** autoimmune (MESH:D001327), POF (MESH:D016649)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12995609/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12995609/full.md

## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC12995609/full.md

---
Source: https://tomesphere.com/paper/PMC12995609