Pathogen recognition receptors, cancer and inflammation in the gut.
Pathogen recognition receptors, cancer and inflammation in the gut.
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DOI：
10.1016/j.coph.2009.09.006
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发表时间：
2009-12
影响因子：
4
通讯作者：
Abreu, Maria T.
中科院分区：
文献类型：
--
作者：
Fukata, Masayuki;Abreu, Maria T.
病原体识别受体（PRR）启动对感染和组织损伤的即时反应，以保护宿主免受微生物入侵。在响应粘膜损伤时，肠道PRR信号启动损伤修复过程。最近的进展似乎将PRR异常与炎症性和肿瘤性肠道疾病联系起来。新出现的证据表明，PRRs具有双重作用，它们可能同时诱导肿瘤发生和抗肿瘤免疫。PRR可能主要通过NF-κB激活细胞存活信号，诱导肿瘤细胞增殖，但该信号可激活树突状细胞，促进抗肿瘤免疫。肿瘤细胞内的TLR信号可能导致逃避免疫监视，转移性生长的繁殖，或者更确切地说，诱导依赖于配体的肿瘤细胞凋亡。上皮细胞在受损或肿瘤转化过程中诱导内源性PRR配体。有针对性地操纵PRR信号可能为许多胃肠道疾病的新治疗策略的发展提供新的机会。
The pathogen recognition receptors (PRR) initiate immediate responses against infection and tissue damage to protect the host from microbial invasion. In response to mucosal damage, intestinal PRR signaling initiates damage repair processes. Recent advances appear to link PRR abnormalities and inflammatory as well as neoplastic intestinal disorders. Emerging evidence suggests a dual role of PRRs in which they may simultaneously induce tumorigenesis and anti-tumor immunity. PRR may induce tumor cell proliferation by activating cell survival signaling mainly via NF-κB, but this signal can activate dendritic cells to promote anti-tumor immunity. TLR signaling within the tumor cells may result in evasion of immune surveillance, propagation of metastatic growth, or rather, induction of tumor cell apoptosis depending on ligands. Epithelial cells induce endogenous PRR ligands when damaged or during neoplastic transformation. Targeted manipulation of PRR signaling may provide emerging opportunities for the development of new therapeutic strategies for many gastrointestinal diseases.
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影响因子：
56.9
作者：
Blander, JM;Medzhitov, R
通讯作者：
Medzhitov, R
DOI：
10.1152/ajpgi.00328.2004
发表时间：
2005-05-01
影响因子：
4.5
作者：
Fukata, M;Michelsen, KS;Abreu, MT
通讯作者：
Abreu, MT
影响因子：
6.2
作者：
El Andaloussi, Abdeljabar;Sonabend, Adam M.;Lesniak, Maciej S.
通讯作者：
Lesniak, Maciej S.
影响因子：
3.1
作者：
Cario, E;Podolsky, DK
通讯作者：
Podolsky, DK
DOI：
10.1093/jnci/dji403
发表时间：
2005-12-07
期刊：
JOURNAL OF THE NATIONAL CANCER INSTITUTE
影响因子：
--
作者：
Bauer, AK;Dixon, D;Kleeberger, SR
通讯作者：
Kleeberger, SR