The critical role of IFNγ in the epidermotropic migration of lymphocytes in oral lichen planus

J Oral Pathol Med. 2023 Jan;52(1):72-80. doi: 10.1111/jop.13383. Epub 2022 Nov 17.

Abstract

Introduction: The chemokines play a crucial role in the recruitment of lymphocytes in oral lichen planus, and the activated epithelial cells are the main producers of the chemokines. However, the signals provoking chemokine secretion still remain to be elucidated.

Methods: The global expression profile of chemokines in oral epithelial cell line induced by IFNγ was determined by microarray analysis. The gene and protein expression was validated in primary culture of oral epithelial cells, and the effects of IFNγ on regulating chemokine production were compared with that of TNFα and IL2. Moreover, the capability of primary culture of oral epithelial cells to attract peripheral lymphocytes in response to IFNγ was investigated in oral lichen planus patients, and the cell phenotype of the recruited lymphocytes was analyzed using flow cytometry.

Results: IFNγ triggered the expression of multiple chemokines in the oral epithelial cells. The expression pattern of the chemokines closely resembled that in the epithelial cell layer of oral lichen planus lesions. Compared with IL2 and TNFα, IFNγ demonstrated a distinct maximal effect on the chemokines secretion in primary culture of oral epithelial cells. The migration of peripheral lymphocytes toward the culture supernatant of IFNγ-treated primary culture of oral epithelial cells was significantly enhanced in the oral lichen planus group compared to that in the healthy control group.

Conclusion: IFNγ plays an important role in the chemokine secretion and epidermotropic migration of lymphocytes in oral lichen planus.

Keywords: CXCL10; CXCL11; CXCL9; chemokine; cytokine.

MeSH terms

  • Chemokines
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-2 / pharmacology
  • Lichen Planus, Oral* / metabolism
  • Lymphocytes
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Tumor Necrosis Factor-alpha
  • Interleukin-2
  • Interferon-gamma
  • Chemokines