may be a central contributor to idiopathic pulmonary fibrosis and a potential target for biomarkers and therapies.
Evidence
This narrative review used a comprehensive but non-systematic PubMed and Web of Science search through October 2025 to synthesize research on aging, immune cell subsets, and IPF.
Caveat
Because the review did not use strict algorithmic inclusion or exclusion criteria, its conclusions map concepts and hypotheses rather than providing systematic evidence of clinical benefit.
Simplified
Idiopathic pulmonary fibrosis (IPF) is a common lung disease among the elderly, which has attracted increasing attention in recent years due to its poor prognosis and limited treatment options. Over the past decade, significant progress has been made in understanding the mechanisms of IPF, establishing it as an age-related disease in which cellular senescence plays a critical role in its pathogenesis and progression. Aging also induces structural and functional changes in the immune system, a process termed , which triggers systemic low-grade chronic inflammation and is likely involved in promoting pulmonary fibrosis. This highlights immunosenescence as a potential core driver of IPF. Consequently, targeting immunosenescence in IPF represents a novel avenue for disease exploration. Given the narrative nature of this review, we conducted a comprehensive but non-systematic literature search. We searched electronic databases (including PubMed and Web of Science) for publications published up to October 2025. The search used combinations of terms related to "IPF" and "Aging". Due to the broad scope of this review, we did not adopt strict algorithmic inclusion or exclusion criteria; instead, we prioritized papers with pioneering significance, high impact studies, and publications that most clearly demonstrated the evolution of concepts and current debates in the field. This paper systematically reviews recent advances in research on immunosenescence in IPF and the roles of relevant immune cell subsets, discussing promising biomarkers for clinical diagnosis and related therapeutic strategies. In the future, further studies are required to elucidate the mechanisms by which immunosenescence contributes to IPF. Employing advanced technologies to identify sensitive biomarkers and develop promising therapeutic approaches is essential to address the current clinical challenges faced by IPF patients.
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