IL-17结构及其信号通路与肿瘤的关系

被引:18
作者
地力下司马义 [1 ]
李锋 [1 ,2 ]
张文杰 [1 ,2 ]
机构
[1] 石河子大学医学院病理学教研室
[2] 石河子大学医学院新疆地方与民族高发病教育部重点实验室
关键词
IL-17; 信号通路; 肿瘤;
D O I
暂无
中图分类号
R730.2 [肿瘤病理学、病因学];
学科分类号
100214 [肿瘤学];
摘要
IL-17的发现已有20年,IL-17由CD4+T细胞分泌的一种细胞因子。TH17细胞分泌的IL-17结合于靶细胞后可以促进炎症趋化因子、急性期蛋白、中性粒细胞聚集,从而在机体免疫和自身免疫性疾病中发挥作用。在风湿性关节炎,系统性红斑狼疮,银屑病等的研究发现在这些疾病中均存在IL-17的高表达,IL-17与其他分子协同作用在自身免疫性疾病的发病机制中具有重要作用。同时在宫颈癌,黑色素瘤,乳腺癌等的研究中均发现存在IL-17的高表达。IL-17可以促进慢性炎症的进展,引起组织增生,促进组织癌变,促进肿瘤新生血管生成。对IL-17及其信号通路的研究深入,可以为肿瘤的分子靶向治疗提供新的思路。
引用
收藏
页码:166 / 171
页数:6
相关论文
共 13 条
[1]
Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis [J].
Tzartos, John S. ;
Friese, Manuel A. ;
Craner, Matthew J. ;
Palace, Jackie ;
Newcombe, Jia ;
Esiri, Margaret M. ;
Fugger, Lars .
AMERICAN JOURNAL OF PATHOLOGY, 2008, 172 (01) :146-155
[2]
Stimulation of the intracellular bacterial sensor NOD2 programs dendritic cells to promote interleukin-17 production in human memory T cells [J].
van Beelen, Astrid J. ;
Zelinkova, Zuzana ;
Taanman-Kueter, Esther W. ;
Muller, Fernke J. ;
Hommes, Daniel W. ;
Zaat, Sebastian A. J. ;
Kapsenberg, Martien L. ;
de Jong, Esther C. .
IMMUNITY, 2007, 27 (04) :660-669
[3]
Human rheumatoid synovial fibroblasts promote osteoclastogenic activity by activating RANKL via TLR-2 and TLR-4 activation [J].
Kim, Kyoung-Woon ;
Cho, Mi-La ;
Lee, Sang-Heon ;
Oh, Hye-Joa ;
Kang, Chang-Min ;
Ju, Ji Hyeon ;
Min, So-Youn ;
Cho, Young-Gyu ;
Park, Sung-Hwan ;
Kim, Ho-Youn .
IMMUNOLOGY LETTERS, 2007, 110 (01) :54-64
[4]
Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis [J].
Capon, Francesca ;
Di Meglio, Paola ;
Szaub, Joanna ;
Prescott, Natalie J. ;
Dunster, Christina ;
Baumber, Laura ;
Gutin, Alexander ;
Abkevic, Victor ;
Burden, A. David ;
Lanchbury, Jerry ;
Barker, Jonathan N. ;
Trembath, Richard C. ;
Nestle, Frank O. .
HUMAN GENETICS, 2007, 122 (02) :201-206
[5]
IL-22 increases the innate immunity of tissues [J].
Wolk, K ;
Kunz, S ;
Witte, E ;
Friedrich, M ;
Asadullah, K ;
Sabat, R .
IMMUNITY, 2004, 21 (02) :241-254
[6]
Interleukin-17 family members and inflammation [J].
Kolls, JK ;
Lindén, A .
IMMUNITY, 2004, 21 (04) :467-476
[7]
Interleukin-17 family and IL-17 receptors [J].
Moseley, TA ;
Haudenschild, DR ;
Rose, L ;
Reddi, AH .
CYTOKINE & GROWTH FACTOR REVIEWS, 2003, 14 (02) :155-174
[8]
Antigen-specific T cell Sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses [J].
Nakae, S ;
Komiyama, Y ;
Nambu, A ;
Sudo, K ;
Iwase, M ;
Homma, I ;
Sekikawa, K ;
Asano, M ;
Iwakura, Y .
IMMUNITY, 2002, 17 (03) :375-387
[9]
Expression of IL-17 mRNA in ovarian cancer [J].
Kato, T ;
Furumoto, H ;
Ogura, T ;
Onishi, Y ;
Irahara, M ;
Yamano, S ;
Kamada, M ;
Aono, T .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 282 (03) :735-738
[10]
Interleukin-17 induces rapid tyrosine phosphorylation and activation of raf-1 kinase in human monocytic progenitor cell line U937 [J].
Subramaniam, SV ;
Pearson, LL ;
Adunyah, SE .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 259 (01) :172-177