TLR4‐induced B7‐H1 on keratinocytes negatively regulates CD4+ T cells and CD8+ T cells responses in oral lichen planus. Issue 5 (14th February 2017)

• Record Type: Journal Article
• Authors: Zhang, Jing; Tan, Ya‐qin; Wei, Ming‐hui; Ye, Xiao‐jing; Chen, Guan‐ying; Lu, Rui; Du, Ge‐fei; Zhou, Gang
• Is Part Of: Experimental dermatology. Volume 26:Issue 5(2017)
• Page Start: 409
• Page End: 415
• Publication Date: 2017-02-14
• Subjects: B7‐H1 -- CD4+ T cells -- CD8+ T cells -- keratinocytes -- oral lichen planus -- TLR4; Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.13244
• Languages: English
• ISSNs: 0906-6705

Abstract

Abstract: Oral lichen planus (OLP) is a T‐cell‐mediated autoimmune mucocutaneous disease affected by the interactions among the keratinocytes, CD4 + T cells and CD8 + T cells. B7‐H1 induced by Toll‐like receptors (TLRs) can suppress T‐cell immune reaction, thereby resulting in immune tolerance. However, the role of TLR‐mediated B7‐H1 on keratinocytes in the immune response of OLP is still unknown. The present study showed that TLR4 could induce time‐coursed B7‐H1 expression on oral keratinocytes, and blocking NF‐κB or PI3K/mTOR pathway downregulated B7‐H1 transcriptional expression. Moreover, TLR4‐stimulated oral keratinocytes inhibited the proliferation of OLP CD4 + T cells and OLP CD8 + T cells, and simultaneously prompted their apoptosis. Blockade of keratinocyte‐associated B7‐H1 restored the declined proliferation of OLP CD4 + T cells and OLP CD8 + T cells, and prevented their increased apoptosis. Therefore, TLR4‐upregulated B7‐H1 on keratinocytes could decelerate immune responses of CD4 + T cells and CD8 + T cells in OLP.