The Mechanism of Immune Intervention by Iguratimod in Oral Lichen Planus Patients: An In Vitro Experimental Study.

Background: Oral lichen planus (OLP) is a T cell-mediated immune disease. Iguratimod (IGU) is a novel immunomodulatory agent for rheumatoid arthritis. No studies have been reported on the mechanism of IGU in the treatment of OLP, which deserves investigation.

E. coli LPS/TLR4/NF-κB Signaling Pathway Regulates Th17/Treg Balance Mediating Inflammatory Responses in Oral Lichen Planus.

Oral lichen planus (OLP) is a chronic inflammatory autoimmune disease mediated by T cells. The imbalance of microflora has potential impacts on the onset and development of OLP, but the mechanism is still unclear. Here, we investigated the effects of Escherichia coli (E.

MiR-155-5p modulates inflammatory phenotype of activated oral lichen-planus-associated-fibroblasts by targeting SOCS1.

Background: Oral lichen planus (OLP) is a chronic inflammatory oral mucosal disease. Cytokines are closely associated with OLP development. In addition to immune cells, fibroblasts have been reported to induce regional inflammation.

FAP-α immunofibroblasts in oral lichen planus promote CD4 T-cell infiltration via CCL5 secretion.

Oral lichen planus (OLP) is a T cell-mediated, chronic inflammatory disease. CD4 T-cell infiltration plays a crucial role in the pathogenesis of OLP. Fibroblasts are activated under pathological conditions and perform various functions.

Cross-talk between CXC chemokine ligand 10-CXC chemokine receptor 3 axis and CC chemokine ligand 17-CC chemokine receptor 4 axis in the pathogenesis of oral lichen planus.

Objectives: This study aimed to determine whether a correlation existed between CXC chemokine ligand 10 (CXCL10)-CXC chemokine receptor 3 (CXCR3) and CC chemokine ligand 17 (CCL17)-CC chemokine receptor 4 (CCR4) in the pathogenesis of oral lichen planus (OLP).

Methods: Peripheral blood of OLP patients (non-erosive and erosive groups) and healthy controls were collected, and T cells were isolated and purified. T cells were co-cultured with three groups: blank, anti-CXCR3, and anti-CCR4.