LPS-miR-34a-CCL22 axis contributes to regulatory T cell recruitment in periapical lesions.
LPS-miR-34a-CCL22 axis contributes to regulatory T cell recruitment in periapical lesions.
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DOI：
10.1016/j.bbrc.2015.03.098
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发表时间：
2015-05
影响因子：
3.1
通讯作者：
M. He;Guangtai Song;Yanqin Yu;Qiuchen Jin;Z. Bian
中科院分区：
文献类型：
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作者：
M. He;Guangtai Song;Yanqin Yu;Qiuchen Jin;Z. Bian
调节性T细胞(Tregs)已被证明在根尖周病变中调节免疫反应和控制对感染的防御，但Tregs被招募到这些病变中的潜在机制尚不清楚。在这里，我们证明了编码CCL22(也称为巨噬细胞衍生趋化因子)的基因在实验性根尖周病变的进展过程中在根尖周组织中的表达上调，这种上调与病变中积累的Tregs的数量呈正相关。在机制方面，我们确定了内毒素通过抑制miR-34a上调巨噬细胞Ccl22的表达。这些发现提示，脂多糖-miR-34a-CCL22轴可能参与了Tregs在根尖周病变中的募集，为控制本病提供了一个潜在的治疗靶点。
Regulatory T cells (Tregs) have been shown to regulate the immune response and to control the defense against infection in periapical lesions, but the underlying mechanisms by which Tregs are recruited to these lesions remain unknown. Here we demonstrate that expression of the gene encoding CCL22 (also known as macrophage-derived chemokine), the major chemoattractant that recruits Tregs, is upregulated in periapical tissue during the progression of experimental periapical lesions; this upregulation positively correlated with the number of Tregs that accumulated in the lesions. In terms of mechanism, we determined that lipopolysaccharide (LPS) up-regulatesCcl22expression in macrophages by suppressing miR-34a. These findings suggest that the LPS-miR-34a-CCL22 axis may contribute to the recruitment of Tregs in periapical lesions, providing a potential therapeutic target for controlling this disease.