Conclusions
T-reg expansion in the localized inflammatory TME leads to a failure of immune regulation by suppressing antitumor response, which can be a latent and significant factor contributing to LCH progression. However, T-reg may also acquire the capability for aiding in initiating T-cell responses under the "cytokine storm" at the beginning of LCH onset. T-reg might contribute to the augmentation of tissue repair by transforming growth factor-β (TGF-β), explaining the self-limiting character of LCH.
Objective
Langerhans cell histiocytosis (LCH) is a rare myeloid-origin neoplasm characterized by the expansion and dissemination of CD1 a+/CD207+ dendritic cells (LCH cells), but the rarity of its occurrence has long impeded progress in understanding its pathology. We focus on the potentially important role that regulatory T cells (T-reg) play in the oral and maxillofacial LCH tumor microenvironment (TME). Study design: Nine cases of oral and maxillofacial LCH, diagnosed from 2009 to 2019, were collected retrospectively from the affiliated hospitals of Southern Medical University. Immunohistochemistry was conducted characterizing T cells and T-reg phenotype. Data were evaluated by 1-sample Wilcoxon's test.
Results
Significantly increased frequency and abnormal distributions of T-reg were identified in all the LCH lesion sections. Proliferating T-reg account for a mean average of 11.5% of the total T-cell subsets, with significant difference (Wilcoxon's test; P < .05). Conclusions: T-reg expansion in the localized inflammatory TME leads to a failure of immune regulation by suppressing antitumor response, which can be a latent and significant factor contributing to LCH progression. However, T-reg may also acquire the capability for aiding in initiating T-cell responses under the "cytokine storm" at the beginning of LCH onset. T-reg might contribute to the augmentation of tissue repair by transforming growth factor-β (TGF-β), explaining the self-limiting character of LCH.