Jing-Ya Yang1, Ya-Qin Tan1,2, Gang Zhou1,2. 1. The 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. 2. Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Abstract
OBJECTIVE: Oral lichen planus (OLP) is a T cell-mediated inflammatory disease with uncertain etiology. Exosomes are cell-derived vesicles containing biological cargo, being associated with the development of multiple inflammatory diseases. The present study aims to investigate the role of T cell-derived exosomes in the pathogenesis of OLP. METHODS: Exosomal marker CD63 was detected in OLP lesions by immunohistochemistry. Twenty-three cytokines in T cell-derived exosomes were assessed using luminex xMAP-based assay. After co-incubating with exosomes, the apoptosis of keratinocytes and the proliferation of Jurkat cells were assessed via flow cytometry and cell counting kit-8 assay, respectively. RESULTS: CD63 was highly expressed in the lymphocyte infiltrated areas of OLP lesions. OLP T cell-derived exosomes contained upregulated interleukin-7, -10, -12, -17 and downregulated interleukin-1β, -5, and interferon-γ. Both exosomes from OLP patients and controls induced the apoptosis of keratinocytes and altered their morphology. Moreover, healthy control-derived exosomes markedly inhibited the proliferation of Jurkat cells, whereas OLP-derived exosomes exhibited no inhibitory effect. CONCLUSIONS: OLP T cell-derived exosomes have an aberrant cytokine profile and could trigger the apoptosis of keratinocytes in vitro, which may be involved in the pathogenesis of OLP.
OBJECTIVE: Oral lichen planus (OLP) is a T cell-mediated inflammatory disease with uncertain etiology. Exosomes are cell-derived vesicles containing biological cargo, being associated with the development of multiple inflammatory diseases. The present study aims to investigate the role of T cell-derived exosomes in the pathogenesis of OLP. METHODS: Exosomal marker CD63 was detected in OLP lesions by immunohistochemistry. Twenty-three cytokines in T cell-derived exosomes were assessed using luminex xMAP-based assay. After co-incubating with exosomes, the apoptosis of keratinocytes and the proliferation of Jurkat cells were assessed via flow cytometry and cell counting kit-8 assay, respectively. RESULTS: CD63 was highly expressed in the lymphocyte infiltrated areas of OLP lesions. OLP T cell-derived exosomes contained upregulated interleukin-7, -10, -12, -17 and downregulated interleukin-1β, -5, and interferon-γ. Both exosomes from OLP patients and controls induced the apoptosis of keratinocytes and altered their morphology. Moreover, healthy control-derived exosomes markedly inhibited the proliferation of Jurkat cells, whereas OLP-derived exosomes exhibited no inhibitory effect. CONCLUSIONS: OLP T cell-derived exosomes have an aberrant cytokine profile and could trigger the apoptosis of keratinocytes in vitro, which may be involved in the pathogenesis of OLP.