The effect of low-temperature-induced immune activation in elderly idiopathic facial palsy: the association between Th1/Th2 imbalance and facial nerve inflammation

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.