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Updated: Oct 17, 2025

Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
Published on: February 16, 2016
Characterization and function of circulating mucosal-associated invariant T cells and γδT cells in oral lichen planus
Jing-Ya Yang1, Fang Wang1,2, Gang Zhou1,2
1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Background:
Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory disease with uncertain aetiology. Mucosal-associated invariant T (MAIT) cells and γδT cells are unconventional, innate-like T cells with immunoregulatory capacity. This study aimed to investigate the potential effects of MAIT and γδT cells on the pathogenesis of OLP.
Methods:
Circulating MAIT cells and γδT cells were identified using flow cytometry. Surface proteins including CD4, CD8, CD69, CD103, CD49d, programmed death-1 (PD-1) and its ligand PD-L1 were assessed. Cytokines containing interleukin (IL)-4, IL-17, interferon (IFN)-γ, granzyme B and tumour necrosis factor (TNF)-α released by MAIT and γδT cells were measured following PMA and ionomycin stimulation.
Results:
Circulating MAIT and γδT cells were deficient in OLP. The percentage of CD4+ , CD69+ , CD103+ and PD-1+ MAIT cells was increased in OLP, while that of CD8+ and CD49d+ MAIT cells was decreased. The percentage of CD103+ , PD-1+ and PD-L1+ γδT cells was upregulated in OLP. Both the MAIT and γδT cells in OLP produced less IL-4 than controls. The granzyme B-producing MAIT cells were increased, while γδT cells secreting granzyme B and TNF-α were reduced in OLP. IL-17 and IFN-γ in OLP MAIT and γδT cells were not significantly different from that in controls. The frequency of OLP MAIT cells and the MAIT/γδT rate were positively associated with the disease severity.
Conclusion:
The deficient MAIT and γδT cells expressing functional proteins and releasing cytokines may play an immunoregulatory role in the pathogenesis of OLP.
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