Authors
Xing Tang, Ziqin Ji, Xueling Xiao, Tongtong Zhu, Shoujen Lan, Yeayin Yen, Xin Shao, Shune Tan, Chao Wang, Jicheng Zhang
Published in
Frontiers in immunology. Volume 17. Pages 1718030. Epub Sep 30, 2026.
Abstract
The pathogenesis of idiopathic facial palsy in the elderly has not been fully elucidated. Recent studies have shown that exposure to low temperatures may participate in the pathological process through immune-mediated pathways. This article reviews that cold stimulation can disrupt the Th1/Th2 immune balance, manifested as reduced secretion of Th1-type cytokines and upregulation of Th2-type cytokines, thereby inducing peripheral inflammatory responses around the facial nerve, leading to nerve edema, demyelination, and conduction dysfunction. Due to the immune aging characteristics of the elderly population, including the reduction of the initial T cell pool, the imbalance of pro-inflammatory and anti-inflammatory factor ratios, and the decline in regulatory T cell function, they are more sensitive to the immune dysregulation induced by low temperatures and have a significantly increased risk of facial palsy. Clinical and animal experimental evidence supports this mechanism, suggesting that the serum IL-4/IFN-γ ratio may serve as a prognostic marker. Future multi-center studies are needed to verify the effectiveness of targeted immune regulation intervention through the Th2 pathway and explore the application value of low-temperature warning and individualized warming strategies in the prevention of facial palsy in the elderly.
PMID:
42876459
Bibliographic data and abstract were imported from PubMed on 15 Oct 2026.
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