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核因子-κB家族成员c-Rel在自身免疫病发病机制及治疗中的研究进展 被引量:3

Advances of transcription factor c-Rel in the pathogenesis and treatment of autoimmune diseases
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摘要 哺乳动物核因子-κB (NF-κB)家族由c-Rel、RelA(p65)、RelB、NF-κB1(p50/p105)以及NF-κB2(p52/p100)五名成员组成.相比于其它家族成员广泛表达于机体的各种细胞,c-Rel主要在活化的淋巴细胞和单核细胞中表达,并与多种免疫细胞的分化以及炎性因子的表达密切相关,从而在自身免疫病的病理过程中发挥着重要作用. The mammalian nuclear factor-kappaB (NF-κB) family consists of five members:c-Rel、RelA(p65) 、RelB,NF-κB1 (p50/p105) and NF-κB2(p52/p100),each of which is endowed with a distinct set of function not shared by other members,although each member may also perform additional functions common to the family.Unlike other members of the NF-κB family that are ubiquitously expressed,c-Rel is preferentially expressed by inflammatory cells and is used to directly control the expression of multiple inflammatory genes that mediate autoimmune diseases such as autoimmune encephalomyelitis and psoriasis,and its alteration is associated with an increased risk for human inflammatory diseases.Thus c-Rel is not only a pathogenic gene but also a susceptibility gene for autoimmune diseases.
出处 《国际免疫学杂志》 CAS 2015年第3期261-265,共5页 International Journal of Immunology
基金 国家自然科学基金(81471554) 黑龙江省教育厅海外学人资助项目(1251H003) 深圳市知识创新计划(JCYJ20130401170412298),深圳市孔雀创新团队(1110140040347265)
关键词 核因子-KB C-REL 自身免疫病 免疫调控 炎症因子 Nuclear factor-kappa B c-Rel Autoimmune disease Immunoregulation Inflammatory cytokines
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  • 1Foster SL, Hargreaves DC, Medzhitov R. Gene-specific control of inflammation by TLR-induced chromatin modifications. Nature 2007; 447:972-978.
  • 2Tato CM, Mason N, Artis D, et al. Opposing roles of NF- kappaB family members in the regulation of NK cell proliferation and production of IFN-gamma. Int Immunol 2006; 18:505-513.
  • 3Saccani A, Schioppa T, Porta C, et aL p50 nuclear factor-kap- paB overexpression in tumor-associated macrophages inhibits M 1 inflammatory responses and antitumor resistance. Cancer Res 2006; 66:11432-11440.
  • 4Lawrence T, Gilroy DW, Colville-Nash PR, Willoughby DA. Possible new role for NF-kappaB in the resolution of inflam- mation. Nat Med 2001; 7:1291-1297.
  • 5Lawrence T, Bebien M, Liu GY, Nizet V, Karin M. IKKalpha limits macrophage NF-kappaB activation and contributes to the resolution of inflammation. Nature 2005; 434:1138-1143.
  • 6Li Q, Lu Q, Bottero V, et al. Enhanced NF-kappaB activation and cellular function in macrophages lacking lkappaB kinase 1 (IKK1). Proc Natl Acad Sci USA 2005; 102:12425-12430.
  • 7Barton GM, Kagan JC, Medzhitov R. Intracellular localization of Toll-like receptor 9 prevents recognition of self DNA but facilitates access to viral DNA. Nat Immunol 2006; 7:49- 56.
  • 8Wang J, Basagoudanavar SH, Wang X, et al. NF-kappa B RelA subunit is crucial for early IFN-beta expression and resistance to RNA virus replication. Jlmmuno12010; 185:1720- 1729.
  • 9Apostolou E, Thanos D. Virus infection induces NF-kappaB- dependent interchromosomal associations mediating monoallelic IFN-beta gene expression. Cell 2008; 134:85-96.
  • 10Alexopoulou L, Holt AC, Medzhitov R, Flavell RA. Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3. Nature 2001; 413:732-738.

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