Cancer inflammation and regulatory T cells.

Cancer inflammation and regulatory T cells.
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DOI:
10.1002/ijc.25430
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发表时间:
2010-08-15
影响因子:
6.4
通讯作者:
Poutahidis, Theofilos
Poutahidis, Theofilos
中科院分区:
医学1区
文献类型:
--
作者:
Erdman, Susan E.;Poutahidis, Theofilos

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慢性炎症是癌症生长和转移所必需的。因此,减少炎症的因素将消除癌症并恢复组织健康。然而,抗炎CD41调节细胞(Treg)在癌症中的作用是神秘和有争议的。我们最近的数据显示,TREG在癌症中的功能可能与炎症性肠病或多发性硬化症相似,TREG积累但缺乏在炎症条件下恢复组织稳态的效力。有趣的是,生命早期暴露于不同的环境生物增强了抑制癌症的保护性TREG表型。相比之下,在生命早期很少接触的卫生个体遭受调节失调的TREG反馈回路。因此,卫生受试者在以后的生活中患恶性肿瘤的风险增加。这种癌症通过阻断潜在的炎症是可逆的。总之,这些数据有助于解释卫生社会中炎症相关癌症发病率的增加,并确定消除癌症和恢复整体健康的目标。
Chronic inflammation is essential for cancer growth and metastasis. It follows that factors reducing inflammation would abrogate cancer and restore tissue health. However, roles for anti-inflammatory CD41 regulatory cells (TREG) in cancer are enigmatic and controversial. Our recent data reveal that TREG may function in cancer similarly to inflammatory bowel disease or multiple sclerosis, whereby TREG accumulate but lack potency to restore tissue homeostasis under inflammatory conditions. Interestingly, early life exposures to diverse environmental organisms reinforce a protective TREG phenotype that inhibits cancer. In contrast, hygienic individuals with few exposures earlier in life suffer from a dysregulated TREG feedback loop. Consequently, hygienic subjects have increased risk of malignancy later in life. This cancer condition is reversible by blocking underlying inflammation. Taken together, these data help explain increased inflammation-associated cancer rates in hygienic societies and identify targets to abrogate cancer and restore overall health.
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