T cell–derived exosomes induced macrophage inflammatory protein‐1α/β drive the trafficking of CD8+ T cells in oral lichen planus. Issue 23 (27th October 2020)

• Record Type: Journal Article
• Authors: Yang, Jing‐Ya; Zhang, Jing; Lu, Rui; Tan, Ya‐Qin; Du, Ge‐Fei; Zhou, Gang
• Is Part Of: Journal of cellular and molecular medicine. Volume 24:Issue 23(2020)
• Page Start: 14086
• Page End: 14098
• Publication Date: 2020-10-27
• Subjects: exosome -- macrophage inflammatory protein‐1α/β -- migration -- oral lichen planus -- T cell; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.16020
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Oral lichen planus (OLP) is a T cell–mediated chronic inflammatory disease with uncertain aetiology. Exosomes are nanosized particles with biological capacities. Here, we aimed to study the effects of T cell–derived exosomes (T‐exos) on the pathogenesis of OLP and its mechanism. T‐exos were incubated with Jurkat cells for 48 hours, and 26 cytokines in the supernatant were measured by luminex assay. The expression of macrophage inflammatory protein (MIP)‐1α/β was detected using immunohistochemistry and ELISA; that of CCR1/3/5 on peripheral T cells was determined by flow cytometry. Transwell assay was performed to investigate the chemotactic effect of MIP‐1α/β, and cells in the lower chambers were examinated by flow cytometry. As a result, OLP T‐exos elevated the production of MIP‐1α/β, which were highly expressed in OLP tissues and plasma. CCR1/5 were markedly expressed on OLP peripheral T cells, and the majority of CCR1/5 + T cells were CD8 + T cells. Besides, MIP‐1α/β promoted the migration of OLP mononuclear cells, while inhibiting CCR1/5 significantly decreased the trafficking of mononuclear cells, especially that of CD8 + T cells. Conclusively, OLP T‐exos‐induced MIP‐1α/β may drive the trafficking of CD8 + T cells after binding with CCR1/5 in OLP, contributing to the development of OLP.