Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2003 Jul;104(7):494-8.

[Antiinfective host defense mechanism: toll-like receptors and innate immunity]

[Article in Japanese]
Yoshio Takesue  1 , Hiroki Ohge, Mohei Kohyama, Yuuji Imamura, Yoshiaki Murakami, Taijiro Sueda
Affiliations
  • PMID: 12884772

[Antiinfective host defense mechanism: toll-like receptors and innate immunity]

[Article in Japanese]
Yoshio Takesue et al. Nihon Geka Gakkai Zasshi. 2003 Jul.

Abstract

The innate immune system has evolved as the first line of defense against invading microorganisms. The recent discovery of the toll-like receptors(TLRs) has rapidly expanded our knowledge of molecular events that initiate host-pathogen interactions. The TLRs, which are expressed on the surface of cells, involved in innate immune recognition, including macrophages and dendritic cells, have a crucial role in the detection of microbial infection. Signals initiated by the interaction of TLRs with pathogen-associated molecular patterns (PAMPs) induce activation of the inflammatory and antimicrobial innate immune response. Ten members of the TLR family have been identified, and they appear to recognize PAMPs, including lipopolysaccharide, peptidoglycan, and bacterial DNA. There has been considerable interest in how adaptive immune responses are controlled by the innate immune system. Recent studies have suggested that TLRs may control the induction of Th1 responses and that a separate system of recognition regulates the Th2 response. Thus TLR signaling represents a key component in the innate immune response to microbial infection.

PubMed Disclaimer

Similar articles

See all similar articles

Publication types

LinkOut - more resources