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Differentiation of Langerhans Cells from Monocytes and Their Specific Function in Inducing IL-22-Specific Th Cells

Yohei Otsuka1,2, Eri Watanabe1, Eiji Shinya1

  • 1Department of Microbiology and Immunology, Nippon Medical School, Tokyo 113-8602, Japan.

Journal of Immunology (Baltimore, Md. : 1950)
|October 17, 2018
PubMed

Insights

Human skin contains Langerhans cells (LCs) and dermal dendritic cells (DCs). This study reveals that transforming growth factor-beta 1 (TGF-β1) drives LC differentiation, with CD1a on LCs crucial for skin immune barrier maintenance.

Area of Science:

  • Immunology
  • Dendritic Cell Biology
  • Skin Homeostasis

Background:

  • Human skin and mucosal tissues harbor distinct dendritic cell (DC) subsets: epidermal Langerhans cells (LCs) and dermal DCs.
  • LCs express Langerin, while dermal DCs express DC-SIGN, serving as key distinguishing markers.
  • Monocytes differentiate into distinct DC subsets, but environmental cues influencing monocyte-derived LC (moLC) differentiation remain unclear.

Purpose of the Study:

  • To elucidate the role of transforming growth factor-beta 1 (TGF-β1) and other cytokines in Langerhans cell (LC) differentiation from monocytes.
  • To investigate the impact of dexamethasone on monocyte-derived LC (moLC) differentiation and function.
  • To explore the role of CD1a on moLCs in initiating T cell responses and maintaining skin immune barrier function.

Main Methods:

  • Monocyte differentiation into moLCs and moDCs was induced using combinations of GM-CSF, IL-4, TGF-β1, and TNF-α.
  • The effects of dexamethasone on moLC differentiation and expression of Langerin, DC-SIGN, and CD1a were analyzed.
  • Cytokine production by moDCs and moLCs was assessed upon stimulation with specific CD1 ligands, and CD4+ helper T cell responses were measured after CD1a triggering.

Main Results:

  • LC differentiation is dependent on TGF-β1, with IL-4 and TNF-α promoting differentiation into Langerin+DC-SIGN- moLCs, while continuous IL-4 inhibits it.
  • Dexamethasone enhanced TNF-α-induced moLC differentiation and suppressed DC-SIGN expression, leading to CD1a expression, similar to primary LCs.
  • CD1a triggering on moLCs induced IL-22-producing CD4+ helper T cell responses, suggesting a role in skin homeostasis.

Conclusions:

  • TGF-β1 is a critical factor for LC differentiation, modulated by other cytokines and dexamethasone.
  • Dexamethasone promotes LC-like differentiation and influences their functional characteristics.
  • CD1a expressed on LCs plays a significant role in initiating IL-22-mediated immune responses crucial for maintaining the skin's immune barrier.

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