The expression of B7-H1 on keratinocytes in chronic inflammatory mucocutaneous disease and its regulatory role
The expression of B7-H1 on keratinocytes in chronic inflammatory mucocutaneous disease and its regulatory role
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DOI：
10.1016/j.imlet.2004.05.007
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发表时间：
2004-07-15
影响因子：
4.4
通讯作者：
Azuma, M
中科院分区：
文献类型：
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作者：
Youngnak-Piboonratanakit, P;Tsushima, F;Azuma, M
PD-1及其配体B7-H1/PD-L1和B7-DC/PD-L2最近已被鉴定为涉及免疫调节的CD 28-B7家族分子。扁平苔藓（LP）是一种T细胞介导的慢性炎症性皮肤粘膜疾病。我们研究了PD-1及其两种配体在LP中的表达和功能。免疫组化显示PD-1和B7-H1在浸润的T细胞和巨噬细胞中表达丰富，而B7-DC在上皮下巨噬细胞中表达较低。有趣的是，B7-H1在角质形成细胞（KCs）上的大量表达被发现接近于上皮下的大量T细胞浸润。未受刺激的培养KC表达B7-H1和B7-DC，并且它们的表达被促炎细胞因子，特别是IFN-γ上调。IFN-γ处理的KC诱导的T细胞增殖反应和IFN-γ产生优先被抗B7-H1 mAb增强，但不被抗B7-DC mAb增强。这些结果表明B7-H1对KCs与T细胞相互作用的调节作用。我们的研究结果表明，B7-H1对KCs的诱导可能在炎症口腔粘膜和皮肤的耐受诱导中起重要作用。(C)2004 Elsevier B. V.保留所有权利。
PD-1 and its ligands, B7-H1/PD-L1 and B7-DC/PD-L2, have been identified recently as CD28-B7 family molecules that are implicated in immune regulation. Lichen planus (LP) is a T cell-mediated chronic inflammatory mucocutaneous disease. We investigated the expression and function of PD-1 and its two ligands in LP. Immunohistochemical examination revealed the abundant expression of PD-1 and B7-H1 in infiltrating T cells and macrophages, and lower-level expression of B7-DC on macrophages in the subepithelium. Interestingly, substantial expression of B7-H1 on keratinocytes (KCs) was found close to the numerous T cell infiltrates in the subepithelium. Unstimulated cultured KCs, expressed both B7-H1 and B7-DC, and their expression was upregulated by proinflammatory cytokines, particularly IFN-gamma. The T-cell proliferative responses and IFN-gamma production that were induced by IFN-gamma-treated KCs were augmented preferentially by anti-B7-H1 mAb, but not by anti-B7-DC mAb. These results indicate the regulatory role of B7-H1 on KCs in the interactions with T cells. Our results suggest that the induction of B7-H1 on KCs may play an important role in tolerance induction in the inflamed oral mucosa and skin. (C) 2004 Elsevier B.V. All rights reserved.