A possible CD1a Langerhans cell-mast cell interaction in chronic hyperplastic candidosis

Ahmed Ali1, Riina Rautemaa, Jarkko Hietanen

  • 1Department of Anatomy/Biomedicum, University of Helsinki, Helsinki, Finland.

Insights

In chronic hyperplastic candidosis (CHC), CD1a-positive Langerhans cells and RANKL-positive mast cells show altered distribution and activity. This suggests enhanced dendritic cell recruitment and interaction with T lymphocytes, impacting oral immunity.

Area of Science:

  • Immunology
  • Oral Pathology
  • Dermatology

Background:

  • T lymphocyte-antigen-presenting cell (APC) interaction is crucial for immune responses.
  • Langerhans cells (LCs) are key APCs in oral mucosa.
  • Chronic hyperplastic candidosis (CHC) involves persistent Candida infection and immune dysregulation.

Purpose of the Study:

  • To investigate the distribution and characteristics of CD1a-positive Langerhans cells (LCs) in CHC.
  • To examine the presence and localization of receptor activator of nuclear factor kappa B ligand (RANKL)-positive cells in CHC.
  • To understand the role of LCs and RANKL in the pathogenesis of CHC.

Main Methods:

  • Tissue sections of CHC, leukoplakia, and healthy oral mucosa were analyzed.
  • Immunohistochemistry using CD1a and RANKL monoclonal antibodies was performed.
  • Two antigen-retrieval protocols (pepsin and Tris-EDTA heat treatment) were employed.

Main Results:

  • CD1a-positive LCs were found in all epithelial layers, at the basement membrane, and in the lamina propria in CHC, unlike in healthy or leukoplakia tissues.
  • Pepsin digestion revealed mast cell degranulation, indicating RANKL release.
  • LCs exhibited numerical, morphological, and topographical variations in CHC.

Conclusions:

  • Dendritic cell (DC) recruitment into the epithelium contributes to the altered LC profile in CHC.
  • RANK-positive and RANKL-sensitive DCs in CHC have increased opportunities for T lymphocyte interaction.
  • Mast cells are a source of soluble RANKL, suggesting active mast cell involvement in CHC pathogenesis.
Abstract