Toll-like receptors and sepsis

被引:27
作者
Ishii K.J.
Akira S. [1 ,2 ]
机构
[1] Akira Innate Immunity Project, ERATO, Japan Science/Technology Agency
[2] Department of Host Defense, Res. Inst. for Microbial Diseases, Osaka University, Suita, Osaka 565-0871
基金
日本科学技术振兴机构;
关键词
Adaptor Molecule; Endotoxin Tolerance; Related Pathogenesis; Innate Immune Activation; Nonimmune Cell;
D O I
10.1007/s11908-004-0034-1
中图分类号
学科分类号
摘要
Recent evidence suggests that Toll-like receptors (TLRs) play a major role in innate immunity to recognize specific molecular patterns derived from pathogens, including lipid, protein, DNA, and RNA, and to fight against pathogens. Each TLR displays a difference in the expression pattern, intracellular localization, and signaling pathway, resulting in the distinct immune responses. The resultant immune activation augments host resistance to a variety of infectious organisms. However, such responses may exceed the threshold to maintain host homeostasis in the case of sepsis. TLR-mediated innate immune activation also induces several molecles shown to negatively regulate TLR signaling. Thus, TLRs may play an important role in positive and negative regulation of immune responses during sepsis. Copyright © 2004 by Current Science Inc.
引用
收藏
页码:361 / 366
页数:5
相关论文
共 53 条
  • [1] Janeway Jr. C.A., Medzhitov R., Innate immune recognition, Annu. Rev. Immunol., 20, pp. 197-216, (2002)
  • [2] Matzinger P., The danger model: A renewed sense of self, Science, 296, pp. 301-305, (2002)
  • [3] Medzhitov R., Janeway Jr. C.A., Decoding the patterns of self and nonself by the innate immune system, Science, 296, pp. 298-300, (2002)
  • [4] Takeda K., Kaisho T., Akira S., Toll-like receptors, Annu. Rev. Immunol., 21, pp. 335-376, (2003)
  • [5] Akira S., Takeda K., Kaisho T., Toll-like receptors: Critical proteins linking innate and acquired immunity, Nat. Immunol., 2, pp. 675-680, (2001)
  • [6] Riedemann N.C., Guo R.F., Ward P.A., The enigma of sepsis, J. Clin. Invest., 112, pp. 460-467, (2003)
  • [7] Medzhitov R., Preston-Hurlburt P., Janeway Jr. C.A., A human homologue of the Drosophila Toll protein signals activation of adaptive immunity, Nature, 388, pp. 394-397, (1997)
  • [8] Poltorak A., He X., Smirnova I., Et al., Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: Mutations in Tlr4 gene, Science, 282, pp. 2085-2088, (1998)
  • [9] Hoshino K., Takeuchi O., Kawai T., Et al., Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: Evidence for TLR4 as the Lps gene product, J. Immunol., 162, pp. 3749-3752, (1999)
  • [10] Takeuchi O., Sato S., Horiuchi T., Et al., Cutting edge: Role of Toll-like receptor 1 in mediating immune response to microbial lipoproteins, J. Immunol., 169, pp. 10-14, (2002)