The role of dendritic cells in immune regulation of nasal polyps

Histol Histopathol. 2017 Jan;32(1):87-97. doi: 10.14670/HH-11-773. Epub 2016 Apr 27.

Abstract

Nasal polyps (NPs) are caused by a variety of immune cells and inflammatory cells. However, as the most potent antigen-presenting cells in the immune system, the role of dendritic cells (DCs) in NPs is still unclear. In the present research, we studied the role of DCs in immune regulation of NPs. Thirty patients with NPs, who served as the experimental group, received systemic and local glucocorticoids for 4-7 d, and specimens were collected prior to hormone treatment and during surgery. Normal middle turbinate mucosa tissues from 18 patients who underwent nasal septum surgery were collected as controls. The expression levels of CD83, tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4) and eosinophils (EOS) in NP tissues before and after glucocorticoid therapy and in control middle turbinate mucosa tissues were studied. After glucocorticoid therapy, the expression levels of CD83, TNF-α, IL-4 and EOS decreased significantly. In addition, the expression of IL-4 was lower than that of TNF-α, reversing the Th2 cytokine-dominant condition. CD83 and EOS showed a positive correlation. DCs participated in the development and progression of NPs and could promote the generation of Th2 cytokines. After interference by glucocorticoid therapy, DCs could inhibit the expression of Th2 cytokines and induce secretion of Th1 cytokines. DCs and EOS thus might both play roles in promoting the development and progression of NPs, but the underlying mechanism requires further study.

Publication types

  • Clinical Trial

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Dendritic Cells / immunology*
  • Eosinophils / drug effects
  • Eosinophils / immunology
  • Female
  • Glucocorticoids / therapeutic use
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization
  • Interleukin-4 / biosynthesis
  • Male
  • Middle Aged
  • Nasal Polyps / drug therapy
  • Nasal Polyps / immunology*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Young Adult

Substances

  • Glucocorticoids
  • IL4 protein, human
  • Tumor Necrosis Factor-alpha
  • Interleukin-4