Toll-like Receptors in Inflammation

  • Luke A.J. O’Neill
  • Elizabeth Brint

Part of the Progress in Inflammation Research book series (PIR)

Table of contents

  1. Front Matter
    Pages i-xii
  2. Kasper Hoebe, Bruce Beutler
    Pages 1-17
  3. Sandra M. Sacre, Stefan K. Drexler, Brian M. Foxwell
    Pages 19-40
  4. Simon Rothenfusser, Eicke Latz
    Pages 41-61
  5. John W. Hollingsworth, Donald N. Cook, David A. Schwartz
    Pages 63-86
  6. Kathrin S. Michelsen, Terence M. Doherty, Moshe Arditi
    Pages 87-106
  7. Masayuki Fukata, Maria T. Abreu
    Pages 107-123
  8. Ekihiro Seki, David A. Brenner, Robert F. Schwabe
    Pages 125-142
  9. Sinéad E. Keating, Andrew G. Bowie
    Pages 143-171
  10. Andrei E. Medvedev, Douglas B. Kuhns, John I. Gallin, Stefanie N. Vogel
    Pages 173-192
  11. Cecilia Garlanda, Michela Mosca, Alessia Cotena, Virginia Maina, Federica Moalli, Federica Riva et al.
    Pages 213-222
  12. Bruno Conti, Christopher N. Davis, M. Margarita Behrens, Julius Rebek, Tamas Bartfai
    Pages 223-240
  13. Back Matter
    Pages 241-246

About this book

Introduction

Toll-like receptors (TLRs) are critical mediators of the innate immune response in mammals. This family of receptors recognizes a variety of microbial products or motifs and initiates the host response to infection. Examples include TLR4 which recognizes lipopolysaccharide (LPS) from Gram-negative bacteria, TLR3 which recognizes viral double-stranded RNA, and TLR9 which recognizes CpG DNA motifs, found in both viruses and bacteria. All TLRs possess an intracellular region termed the Toll-IL-1 receptor-Resistance (TIR) domain which is essential for signaling from these receptors. The specificity of signaling from individual TLRs arises from differential utilization of adapter proteins. This specificity results in a tailoring of the host defense response depending on the microbe being sensed. TLRs are increasingly being implicated in both infectious and inflammatory diseases, notable examples being sepsis, inflammatory bowel disease, atherosclerosis, and asthma. There is, therefore, great interest in targeting TLRs therapeutically since a disruption of TLR function will result in a decrease in the production of inflammatory mediators. This volume covers our current understanding of TLRs and their role in inflammation. Given the importance of TLRs in the inflammatory process and their emerging role in inflammatory diseases the book is of great interest to researchers working in inflammation and immunology.

Keywords

Sepsis asthma autoimmune disease bacteria bacterial infection cytokine diseases immunology infection inflammation inflammatory bowel disease regulation research resistance viral infection

Editors and affiliations

  • Luke A.J. O’Neill
    • 1
  • Elizabeth Brint
    • 1
  1. 1.Cytokine Research Group, Department of BiochemistryTrinity College DublinDublin 2Ireland

Bibliographic information

  • DOI https://doi.org/10.1007/3-7643-7441-1
  • Copyright Information Birkhäuser Verlag 2005
  • Publisher Name Birkhäuser Basel
  • eBook Packages Biomedical and Life Sciences
  • Print ISBN 978-3-7643-7285-9
  • Online ISBN 978-3-7643-7441-9
  • About this book