TLR 4‐induced B7‐H1 on keratinocytes negatively regulates CD 4 + T cells and CD 8 + T cells responses in oral lichen planus

Oral lichen planus ( OLP ) is a T‐cell‐mediated autoimmune mucocutaneous disease affected by the interactions among the keratinocytes, CD 4 + T cells and CD 8 + T cells. B7‐H1 induced by Toll‐like receptors ( TLR s) can suppress T‐cell immune reaction, thereby resulting in immune tolerance. However,...

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Veröffentlicht in:Experimental dermatology 2017-05, Vol.26 (5), p.409-415
Hauptverfasser: Zhang, Jing, Tan, Ya‐qin, Wei, Ming‐hui, Ye, Xiao‐jing, Chen, Guan‐ying, Lu, Rui, Du, Ge‐fei, Zhou, Gang
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container_end_page 415
container_issue 5
container_start_page 409
container_title Experimental dermatology
container_volume 26
creator Zhang, Jing
Tan, Ya‐qin
Wei, Ming‐hui
Ye, Xiao‐jing
Chen, Guan‐ying
Lu, Rui
Du, Ge‐fei
Zhou, Gang
description Oral lichen planus ( OLP ) is a T‐cell‐mediated autoimmune mucocutaneous disease affected by the interactions among the keratinocytes, CD 4 + T cells and CD 8 + T cells. B7‐H1 induced by Toll‐like receptors ( TLR s) 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 TLR 4 could induce time‐coursed B7‐H1 expression on oral keratinocytes, and blocking NF ‐κB or PI 3K/ mTOR pathway downregulated B7‐H1 transcriptional expression. Moreover, TLR 4‐stimulated oral keratinocytes inhibited the proliferation of OLP CD 4 + T cells and OLP CD 8 + T cells, and simultaneously prompted their apoptosis. Blockade of keratinocyte‐associated B7‐H1 restored the declined proliferation of OLP CD 4 + T cells and OLP CD 8 + T cells, and prevented their increased apoptosis. Therefore, TLR 4‐upregulated B7‐H1 on keratinocytes could decelerate immune responses of CD 4 + T cells and CD 8 + T cells in OLP .
doi_str_mv 10.1111/exd.13244
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B7‐H1 induced by Toll‐like receptors ( TLR s) 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 TLR 4 could induce time‐coursed B7‐H1 expression on oral keratinocytes, and blocking NF ‐κB or PI 3K/ mTOR pathway downregulated B7‐H1 transcriptional expression. Moreover, TLR 4‐stimulated oral keratinocytes inhibited the proliferation of OLP CD 4 + T cells and OLP CD 8 + T cells, and simultaneously prompted their apoptosis. Blockade of keratinocyte‐associated B7‐H1 restored the declined proliferation of OLP CD 4 + T cells and OLP CD 8 + T cells, and prevented their increased apoptosis. 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title TLR 4‐induced B7‐H1 on keratinocytes negatively regulates CD 4 + T cells and CD 8 + T cells responses in oral lichen planus
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