Abstract：
:Lipid A is a strong activator of monocytes to release immune stimulators such as proinflammatory cytokines. Overproduction of inflammatory cytokines such as TNF and IL-6 is known to cause septic shock that frequently leads to multiple organ failure and finally to death. In recent years, Lipid A has also been recognized by a Toll-like receptor, TLR4. Activation of TLR4by LPS or Lipid A triggers signal transduction via the cytoplasmic domain called the Toll/IL-1 Receptor (TIR) domain. Intracellular TIR domain-containing adaptor molecules are involved in the TLR4-mediated signaling pathways. Moreover, a subset of LPS-inducible genes is regulated in two steps by the inducible nuclear protein. Additionally, the TLR4-mediated activation of signaling cascadesis elaborately down-regulated by a number of negative regulators. In this chapter, we discuss the mechanisms of the activation or de-activation program mediated by the Lipid A receptor TLR4.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Yamamoto M,Akira Sdoi
10.1007/978-1-4419-1603-7_6subject
Has Abstractpub_date
2010-01-01 00:00:00pages
59-68eissn
0065-2598issn
2214-8019journal_volume
667pub_type
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journal_title：Advances in experimental medicine and biology
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pub_type： 杂志文章,评审
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更新日期：2012-01-01 00:00:00
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pub_type： 杂志文章
doi：10.1007/978-1-4899-0949-7_1
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pub_type： 杂志文章,评审
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更新日期：2016-01-01 00:00:00
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pub_type： 杂志文章,评审
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journal_title：Advances in experimental medicine and biology
pub_type： 杂志文章,评审
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更新日期：2011-01-01 00:00:00
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更新日期：2010-01-01 00:00:00
