# The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets

## TL;DR

This paper reviews how immune system dysfunction contributes to lung fibrosis and explores new treatment targets.

## Contribution

The paper provides new insights into immune-fibrotic interactions and identifies potential therapeutic targets.

## Key findings

- Immune dysregulation drives myofibroblast activation and fibrosis progression.
- Immunomodulatory therapies show potential to reverse fibrosis in disease models.
- Heterogeneity in immune-fibrotic interactions suggests opportunities for precision medicine.

## Abstract

Pulmonary fibrosis is the converging pathological outcome of chronic inflammatory lung diseases with diverse etiologies. Sustained inflammation disrupts immune cell homeostasis, driving aberrant activation and differentiation of myofibroblasts and leading to excessive extracellular matrix deposition within the lung interstitium. Emerging evidence indicates that immune dysregulation contributes to myofibroblast activation, and that immunomodulatory therapies may reverse fibrotic progression across diverse disease models. In this Review, we dissect the mechanisms by which immune dysregulation promotes fibrosis in distinct pathological contexts, highlighting the heterogeneity of immune–fibrotic interactions. We further discuss emerging targets with potential for precision intervention, aiming to inform the development of adjunctive and personalized therapeutic strategies.