Skip NavigationSkip to Content

Cooperation of Toll-like receptor signals in innate immune defence

  1. Author:
    Trinchieri, G.
    Sher, A.
  2. Author Address

    NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA. NIAID, Immunobiol Sect, Parasit Dis Lab, Bethesda, MD 20892 USA.;Trinchieri, G, NCI, Canc & Inflammat Program, Ctr Canc Res, Bldg 560,Room 31-93, Frederick, MD 21702 USA.;trinchig@mail.nih.gov asher@niaid.nih.gov
    1. Year: 2007
    2. Date: Mar
  1. Journal: Nature Reviews Immunology
    1. 7
    2. 3
    3. Pages: 179-190
  2. Type of Article: Review
  3. ISSN: 1474-1733
  1. Abstract:

    The mechanisms by which the recognition of Toll-like receptor (TLR) ligands leads to host immunity remain poorly defined. It is now thought that to induce an effective immune response, microorganisms must stimulate complex sets of pattern-recognition receptors, both within and outside of the TLR family. The combined activation of these different receptors can result in complementary, synergistic or antagonistic effects that modulate innate and adaptive immunity. Therefore, a complete understanding of the role of TLRs in host resistance to infection requires 'decoding' of these multiple receptor interactions. This Review highlights recent advances in the newly emerging field of TLR cooperation and discusses their implications for the development of adjuvants and immunotherapies.

    See More

External Sources

  1. DOI: 10.1038/nri2038
  2. WOS: 000244480400011

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel