T cell–derived exosomes induced macrophage inflammatory protein‐1α/β drive the trafficking of CD8+ T cells in oral lichen planus

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 incubate...

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Published inJournal of cellular and molecular medicine Vol. 24; no. 23; pp. 14086 - 14098
Main Authors Yang, Jing‐Ya, Zhang, Jing, Lu, Rui, Tan, Ya‐Qin, Du, Ge‐Fei, Zhou, Gang
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.12.2020
John Wiley and Sons Inc
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Summary: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.
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content type line 23
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.16020