Inhibiti on of T-Cell-Mediated and Infection-Ind uced Periodontal Bone Resorption by TAC E Blockade
Inhibiti on of T-Cell-Mediated and Infection-Ind uced Periodontal Bone Resorption by TAC E Blockade
复制标题
TAC E 阻断对 T 细胞介导和感染诱导的牙周骨吸收的抑制
DOI:
10.1007/978-4-431-54070-0_45
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发表时间:
2012
期刊:
影响因子:
--
通讯作者:
M
中科院分区:
文献类型:
--
作者:
Kanzaki;H.; Han;X.; Asami;Y.; Suzu ki;M.; Kawai;T.; Taubman;M
Host immune responses trigger promotion of bone resorption in periodontitis, and infiltrated lymphocytes express abundant RANKL, the essential factor for osteoclastogenesis. Since RANKL is initially produced as a membrane-bound protein, cell-to-cell contact can be required for osteoclastogenesis. However, distance between lymphocytes and active osteoclasts is generally observed. This observation presume released cytokine(s) from activated lymphocytes might induce osteoclastogenesis in periodontitis.Previously, we reported that cleavage of RANKL and TNF-α by TNF-α converting enzyme (TACE) from lymphocytes can play a role in human periodontitis. Herein, we further examined function of TACE in two experimental periodontitis models in rats: (1) Aggregatibacter actinomycetemcomitans-reactive T-cell adoptive transfer and (2)Porphyromonas gingivalisinfection. Anti-TACE antibody was injected into the gingivae to probe the role of TACE in bone destruction. Our data suggested that TACE blockade could inhibit alveolar bone destruction. TACE might be a potentially therapeutic target for periodontitis amelioration.